Caries of deciduous teeth in children

Caries of deciduous teeth in children. Patterns of clinical manifestations and course. Diagnosis, differential diagnosis.

Caries of permanent teeth in children. Patterns of clinical manifestations and course. Diagnosis, differential diagnosis.

Dental caries (caries dentis) – a pathological process that develops after teething and is characterized by demineralization and destruction of hard tooth tissue with subsequent formation of a defect in a cavity. According to the WHO nomenclature for the assessment of staggered teeth caries using three basic indicators: prevalence, intensity and increase the intensity of caries.

The prevalence of caries – is the ratio of people ( as a percentage ) that are carious , sealed and removed teeth, ¬ tion to the total number of patients. The prevalence of caries in different ages varies vschobrazhena This pattern of caries in the age curve (Fig. 25). Carious lesions are diagnosed in children aged 1-1.5 years . At the age of 7-9 years, the prevalence of caries increases to 95-100% in children 11-12 years decreases to 70-80 % due to physio ¬ logical change of teeth and the formation of permanent occlusion . Since 13-14, the prevalence of caries years growing again.

         Intensity decay (caries index) – the number of carious teeth removed and sealed in a single surveys. In children with tymcha sovym bite caries index referred to as “CP” (carious, seals ¬ ated) as deleted temporary teeth to be recorded. In children with varying dental occlusion index referred to as CPV + kp (take into account yuhsya affected by caries as temporary and permanent teeth). In children with permanent occlusion of caries index is designated as CPV (carious, sealed, removed).

 

Мал. 25. Вікові періоди високого та низького приросту карієсу зубів

 

         Таблиця 18. Оцінка інтенсивності карієсу зубів за віком (за умови зниженого вмісту фтору в питній воді)

Age, years	The level of caries
	Very High	High	Low	Resistant to decay
2	3 and more	2	0	0
3	6	2-5	1	0
4	9	3-8	2	0
5	9 more kp 1KPV	4-8	1-3
7	10 more kp	7-9 CP 1-4 CPV	1-6 СP	0
9	10 and more 5 and kp CPV more	6-9 kp3-4 CPV	0-5 kp 0-2 Cpv	0
11	8 CPV and more	5-7 CPV	1-4CPV	0
13	12 and more	6-11	1-5	0
15	15 and more	9-14	3-8	0-2
17	18 and more	9-17	4-8	0-3
19	21-32	14-20	7-13	0-6
20-24	26-32	18-25	9-17	0-8
25-29	28-32	20-27	12-19	0-11
30-34	28-32	20-27	13-19	0-12
35-39	29-32	22-28	14-21	0-13
40-44	32	22-32	14-21	0-13

 

As an indicator of the intensity of dental caries , along with an index that takes into account the affected teeth removed and applied index, which takes into account the number of caries -affected surfaces of teeth – Cpt. To determine the index counts the number affected by caries or tooth surfaces sealed . This index more accurately reflects the dynamics of the caries process , which is especially important in determining the effectiveness of preventive measures.

For evaluation of these processes ( dynamics caries development and its effective prevention) used indicator of intensity of growth – decay. To determine the intensity of the su ¬ Hazel ( the index of dental caries or tooth decay index surfaces) in the same person or contingent after a certain period ( 1-3-5 years). The difference in value of the index between the second and the first survey is increase the intensity decay.

 

Etiology

To explain the etiology and pathogenesis of dental caries suggested about 400 theories, the most famous of which contributed to the accumulation of information that allow to express a complete view of the problem.

Without going into detail on all existing theories are given below that at least to some extent, give an explanation of the origin of the most common pathological process – caries.

Theories of the origin of dental caries

1. Chemical-parasitic theory of caries Miller (1884). At one time this teoriyab Ula progressive, was recognized and fairly widespread. Nowadays, the theory of tooth decay was the basis for the modern concept of the pathogenesis of dental caries. According to this theory, the carious destruction occurs two stages:

a) demineralization of dental hard tissues . Lactic acid is formed in the mouth , resulting in lactic acid fermentation of carbohydrate food residue dissolves inorganic substances enamel and dentin ;

b) is the destruction of organic matter dentin proteolytic enzymes of microorganisms.

However, factors such as microorganisms and acids , Miller acknowledged the existence of predisposing factors . He pointed out the role of the quantity and quality of saliva, factor supply, drinking water, emphasized the importance of hereditary factors and conditions of formation of enamel.

2. Physico-chemical theory of caries DA Entin (1928). Entin proposed the theory of decay obtained from the physico- chemical properties of saliva and tooth. He believed that the tooth is semi-permeable membrane through which the osmotic currents caused by the difference in osmotic pressure between two media in contact with the tooth , blood and saliva from the inside out. According to him, under favorable conditions, osmotic currents are centrifugal direction and ensure the normal supply conditions dentin and enamel and prevent action on the enamel of unfavorable factors. In turn, the centripetal movement of substances , ie the surface of the tooth to the pulp was considered abnormal and little direct connection with diseases of the nervous and endocrine systems, heredity , disturbance of mineral metabolism , conditions harchevannya , life , work, physiological relationships that lead to violations pulp in the system – tooth – saliva. Under adverse conditions centrifugal direction osmotic currents weakened and becomes centripetal direction that gives the power of enamel and facilitates action it harmful external agents ( microorganisms) , causing cavities.

Disadvantages theory Entin did not know that at the centripetal flow of substances in enamel occurs nutrition enamel minerals from saliva , and this method is based exogenous caries prevention – covering ftorlaka teeth , causing remineralyzuyuchyh substances ( applications) on the surface of the enamel with a view to refill their enamel – remterapiya , as well as methods of treatment of caries in stage spots : application to the affected area of enamel remineralizuyuchyh substances. 

The scheme of the pathogenesis of dental caries by DA Entin

 

3. The biological theory of caries IG Lukomsky (1948). The author of this theory believed that endogenous factors such as lack of vitamins D, B, and inadequate and poor value for calcium , phosphorus, fluoride in the diet , lack of or insufficient ultraviolet rays break the mineral and protein metabolism. The result is disease odontoblasts that first weakened and then are inferior. Reduces the size and number of odontoblasts , leading to metabolic disturbances in the enamel and dentin . First comes dyskaltsynatsiya , then a change in the composition of organic matter. The theory has no experimental evidence. The negative aspects of this theory: there is no evidence that the odontoblasts are trophic centers of the tooth , theory does not explain the role of sugar in the development of caries, carious lesions and localization preventive effect of fluoride , not proven to be defective in odontoblasts caries . Even in a healthy tooth contact can be found degeneration of odontoblasts in the form of vacuolization and atrophy.

4. Theory of AE Sharpenaka (1949). Sharpenak explained the cause of tooth decay tooth enamel local depletion of proteins as a result of their rapid decay and slow resynthesis , which inevitably leads to caries in a stage of white spots. Slowing resynthesis caused by the absence or low content of amino acids such as lysine and arginine, and the reason for enhancement of proteolysis is a high ambient temperature , hyperthyroidism , nervous overstimulation , pregnancy , tuberculosis , pneumonia , accumulation of acids in the tissues of the body (in particular, insufficient flow of vitamin group, tissues accumulate a large amount of pyruvic acid) , which leads to increased protein breakdown. Kariesogennoy effect of carbohydrates Sharpenak explains that when a large of learning increases the need for vitamin B1, which can cause vitamin deficiency and increased proteolysis in solid substances tooth. Disadvantages theory: not confirmed experimentally that when caries in a stage of degeneration begins proteolysis of proteins , author underestimated the role of microorganisms kariesogennoy local factors and overestimated the role of common factors.

5. Proteolysis-decay theory helatsionna Shattsa and Martin (1956 р). The authors explain the perception of enamel to caries stable calcium -protein complexes. Tooth enamel is the integral structure of the body, which is due to the functional features of mineralized than other tissues. Thus the mineral and organic components of the enamel are in close biochemical connection. The stability of the latter may be affected by penetrating the enamel of different active chemical agents including proteolytic . The development of the caries process is considered in two stages:

a) proteolysis in which the break bonds between proteins and minerals enamel

due to the action of proteolytic enzymes on bacterial protein components ;

b) helatsiya when there is destruction of the mineral part of dental hard tissues due to the formation of complex compounds of metal ions with anions of acids, salts of organic acids , amino acids , proteins and intermediates decay.

Disadvantages theory: there is currently no evidence of the first phase of the caries process by Shattsu – Martin . At the stage of caries spots or breach of covalent bonds between organic and inorganic substances , or protein breakdown have been identified. Underestimated local action of acids produced during dental plaque and overrated helatsionnyy method demineralization of enamel, which is very slow, while the destruction of dental hard tissues is sometimes a very intensive. The theory does not explain the localization of caries lesion frequency specific tooth surfaces.

6. Trofonevrotychna Theory EE Plato. By this theory, considered as trofonevrotychnyy caries process, which , in his opinion , develops only when the power supply is broken dental hard tissues. The main pathogenetic factor EE Plato believed trophic disorders of the nervous regulation of dental tissues. But today we know that teeth with pulp removed in time to 17 years continue to function normally. Removing the pulp as a method of treatment of complicated forms of caries does not lead to structural and functional changes in the enamel of the tooth , the latter continues to function as a full body. Constant dynamic interaction with oral fluid provides hard tissues of the tooth depulpovanoho high mineralizovanist , which corresponds to high acid stability , microhardness and structural homogeneity.

The modern concept of the etiology of dental caries.

Based on historical theories are being made ​​significant progress in the study of the etiology and pathogenesis of dental caries. Generally accepted mechanism of caries is a progressive demineralization of dental hard tissues under the influence of organic acids, the formation of which is connected with the activity of microorganisms. In the event of the caries process involved many etiological factors, allowing polietiolohychnym count caries disease.

The main etiological factors are:

1. Oral cavity;

2. The nature and diet, fluoride content in water;

3. The quantity and quality of saliva;

4. The general condition of the body;

5. Extreme action on the body.

All of the above factors were identified kariesogennoy and subdivided into general and local, such that play an important role in the occurrence of dental caries.

General factors:

1. Inadequate diet and drinking water;

2. Somatic diseases, changes in the functional state of organs and systems during the formation and maturation of tissues.

3. Extreme action on the body;

4. Heredity, causing the usefulness of the structure and chemical composition

tissues. Adverse genetic code.

Local factors:

1. Dental plaque and plaque that is isolated microorganisms;

2. Violation of the composition and properties of oral fluid;

3. Hydrocarbons sticky food residues mouth;

4. Resistance dental tissue caused complete structure and chemical composition of dental hard tissues;

5. Abnormalities in the biochemical composition of dental hard tissues and defective structure of tissues;

6. State dental pulp;

7. State of dentition during bookmarks, development and eruption of permanent teeth.

Kariesogennoy situation is created when any kariesogennoy factor or group acting on the tooth , making it susceptible to acids. Of course, the trigger is the oral cavity with obligatory presence of carbohydrates and touch two factors of tooth structure .

In terms of lowered resistance of dental tissues kariesogennoy situation develops easier and faster.

Clinically the mouth kariesogennoy situation is the following symptoms:

1. Poor oral hygiene;

2. Abundant plaque ;

3. Plaque ;

4. Overcrowding of the teeth and bite abnormalities ;

5. Bleeding gums.

Stability of dental caries or tooth decay resistance provided by:

1. The chemical composition and structure of enamel and other tissues ;

2. The presence pellikuly ;

3. The optimum chemical composition of saliva and myneralizuyuschoyi its activity;

4. Sufficient amount of oral fluid ;

5. A low level of permeability of tooth enamel ;

6. A good chewing load and self-cleaning surfaces of the teeth ;

7. Properties of plaque ;

8. Good oral hygiene ;

9. The features of the diet;

10. Correct formation of primordia and the development of dental tissues ;

11. Timely and complete maturation of enamel after eruption of the tooth;

12. Specific and nonspecific protective factors of the oral cavity .

Susceptibility to caries or tooth karyyesspryymannya contribute:

1. Defective maturation of enamel;

2. A diet deficient proteins , macro -and micronutrients , excess carbohydrates;

3. Water from the lack of fluoride ;

4. Lack pellikuly ;

5. The composition of oral fluid , its concentration , viscosity, amount and rate of discharge;

6. Biochemical composition of hard tissues , which determines the course of caries as a dense structure of spaces with minimal lattice slows the progress of tooth decay and vice versa;

7. State of the neurovascular bundle ;

8. The functional state of organs and systems during the formation and maturation of tissues ;

9. Improper development of the tooth due to common somatic diseases.

In Table. 19 presents some general and local factors charac ¬ Theroux that cause caries in children.

Table 19. Global and local causes of tooth decay in children

General kariesogennoy factors	Local kariesogennoy factors	Impaired resistance of dental tissue
Defective	pathogenic organisms	Inadequate
food;	plaque;	structure;
low content of fluoride in	change the quantitative and	variations in the chemical
water;

 

According to modern concepts , the development of tooth decay occurs vnas ¬ lidok complex interaction of internal and external factors that imple ¬ zuyetsya microorganism in the system – saliva – the structure of the enamel (Fig. 26).

The effect of these factors is easier to figure out if the normal state of enamel seen as a dynamic equilibrium between the constant process of de- and remineralizatsp . In the case when the dental tissues processes Deming – ralizatsiyi outweigh remineralization occurs demi – site neralizatsii as carious spots. Further progression of the process ¬ demiyiyieralizatsiyi enamel and dentin leads to the formation of brown ¬ oznoyi cavity.

It is known that the development of dental caries associated microflora , among which the leading role played by streptococci, especially Str. mutans. Etiological role of microorganisms in the development of dental caries demonstrated in experiments on animals hnotobiotychnyh who have not decay occurred despite prolonged exposure to kariesogennoy diet. Launching kariesogennoy ordinary food microflora of the oral cavity ¬ us human constant led to the development of caries in experimental animals.

Kariesogennoy action of microorganisms associated with the formation of their dental plaque . It is a conglomerate backbone is made up of micro ¬ organisms polysaccharide fixed in the stroma , which to varying degrees in ¬ saturated with minerals . Dental plaque is flat against the tooth surface and is over pelikuloyu – ¬ tion of organic thin film that covers the tooth enamel. Dental plaque is most peo ¬ ple contains the same basic types of microorganisms in different ratios (Table 20). Thus the fate of streptococci (mutans, salivarius, mitis, sangvis) accounts for about 40 % of the total microbial plaque.

 

Table 20. The microflora of dental plaque (by Ch. Moutoun, 1993)

Type of microorganism	Percentage of total NUMBER	The frequency allocation, %
Streptococci	17-38	100
Gram (+) Sticks	22-52	100
Neissena	0-2	99
Gram (-) anaerobic sticks	1-13	94
Fusobactena	0-17	98
Veilonella	0-7	55

 

         Most kariesogennoy th Str. mutans, which produces only lactic acid from glucose , mannitol and sorbitol splits , forming glycans of sucrose. Loss of ability to produce glycans leads to loss of virulence Str. mutans.

The formation of dental plaque occurs in the sequence:

1) the attachment of bacteria to pelikuly ;

2) the formation zovnishnokli hospitable structure ( matrix );

3) the growth of bacteria and the formation of plaque .

There are various mechanisms of attachment of bacteria to pelikuly . LM.Silverstone ( 1980) points to the existence of such phases in this process :

– Adsorption mikromolekul ;

– Chemical attachment of bacteria cell ;

– Return fixing bacteria on the surface;

– Clinched their fixation ;

– Develop secondary microflora.

Chart. 26. Figure Keyes (1962), which reflects the interaction between the three bases ¬ them etiological factors of dental caries

This issue pay much attention to the fact that fixing bacteria reduction will reduce the potential for kariesogennoy in ¬ upper tooth.

Formation matrix associated with the activities of microorganisms. Matrix consists of two components : proteins, glycoproteins mainly derived from saliva, and bacterial extracellular policy ¬ harydiv (mainly carbohydrate polymers ).

For thickening and ” maturation ” of porous and permeable ¬ f us ” young ” dental plaque creates anaerobic conditions that change ¬ tion of microbial composition . The formation of dental plaque is largely due to the disposal of bacteria food debris trapped on the surfaces of the teeth. Most bacteria use substances that readily penetrate the plaque : sucrose , glucose, fructose, mal ¬ tozu , lactose. Of particular importance nadastsya dextran , because the number of significant ¬ adhesive properties required for the fixation and growth of dental plaque , the poorly soluble polysaccharide ¬ priorities would need to resistant microorganisms.

Glycolysis carbohydrates ( sucrose , glucose, fructose ) contributes lo ¬ radical reduction of the pH on the surface of the tooth enamel to a critical level (pH = 5.0 ), accompanied by an increase in the permeability of enamel (Fig. 27). Prolonged maintaining a critical level of hydrogen ions occurs acid dissolution apahytiv surface in the least stable parts of the enamel ( line Rettsiusa , mizhpryzmovi spaces ), accompanied by the penetration of acids in the subsurface layer of enamel demineralization its next.

 

Chart. 27. The process of acid from the interaction between bacteria and kariesogennoy carbohydrates (sucrose). Prevalence of enamel demineralization processes in case of lack of local mechanisms for neutralizing acids (by Ch.Moutoun,1993)

VK Leont’yev and AI Vershinin (1991) suggest a parallel ¬ ing course

two reactions: hydroxyl uhvoryuyetsya is not 10, and 9 atoms Ca2 ^ one of them is substituted for a hydrogen ion (H ^ or hydronium (HgO ^). hydroxyapatite The structure is not destroyed, but decreases its ability to resist acids due a reduction of calcium ¬ tion and therefore calcium-phosphorus coefficien.

Changes in the surface layer of enamel are less pronounced than in the deeper parts of it, due to its structural features (presence of large amounts of fluorapatite) and reminera-ation processes that occur continuously as a result of receipt of the mineral component of oral fluid. The subsequent formation of organic acids on the surface of enamel demineralization leads to increased and gradually increase mikroprostoriv between crystals of enamel prisms. As a result, the conditions for the penetration of microorganisms and their metabolic products of micro-defects of enamel. The source of acid is transferred within the enamel. At this stage of demineralization of enamel caries process extends both along the surface and at depth, forming a cone-shaped cell destruction. Continued existence of areas of demineralization leads to the dissolution of the surface, more resistant enamel layer to form a defect. Consequently, the initial clinical caries enters surface.

Also kariesogennoy action of dental plaque, are important factors that contribute to resistance or susceptibility to dental caries (transferred and related diseases, malnutrition, etc.., Figure 3). Established that in adults and children who have suffered acute infectious disease or suffer from chronic diseases of internal organs and systems, especially often caries. The degree of infestation caries is not associated with one or other person  portunities transferred or concomitant disease.

For various diseases accompanied by increased susceptibility to caries, general him with the fact that they are characterized by changes in the state of immunological reactivity. These changes are primarily in reducing the number and functional activity of cellular and humoral protective factors in both serum and oral fluid in his Principles humoral factor in local anti-infective resistance of the mucous membrane of the mouth is IgA, specifically secretory (S IgA). They prevent adhesion of microorganisms to the mucosal surface of the oral cavity, as well as the dental hard tissues. In addition, S IgA saliva can alter metabolism of microorganisms to limit the formation of colonies, to reduce the virulence of infectious agents.

The development of dental caries is associated with a decrease in the number or absence of S IgA in saliva. However, this view is not shared by all investigators. The contradictory data on the role of S IgA in the pathogenesis of dental caries due to the fact that the system of secretory antibody labile and depends on many factors, local and general (gender, age, climatic conditions, etc.).

Chronic diseases of internal organs and systems are also accompanied by changes in physical and chemical properties of saliva, decreasing its protective and remineralizuyuchoho potential.

Stability of dental caries is defined as the composition and properties VOST enamel. The structure of the enamel as temporary and permanent teeth conditioned primarily by genetic factors, but largely depends on the usefulness of enamel mineralization processes (as vnutrishnoschelepnoyi and oral). It is known that mineral ation of deciduous teeth occurs almost entirely in intra-shnoutrobnyy period as crucial health of the mother during pregnancy. On the stability of deciduous teeth caries significantly affect toxaemia of pregnancy, carbohydrate metabolism, thyroid disease, digestive tract viral illness like chronic hypoxia and others. In the temporary teeth of children born to mothers with the above pathology during pregnancy, caries faultpeared almost immediately after their eruption.

In odontohenez deciduous teeth, and hence on the structure of enamel influenced by factors such as prematurity pregnancy, illnessnewly born and children 1 year of life. Results polarization opcal and X-ray analyzes of deciduous teeth indicate that at physiological pregnancy occurs povnotsin ¬ on mineralization of enamel. In toxemia of pregnancy (nephropathy, sudyanka, preeclampsia, etc.). Enamel of primary teeth revealed some areas of defective mineralization. These sites are stored in infancy, even in intact temporary teeth as hipomineralizovanyh zones.

In mineralization of permanent teeth in children than the mother’s health significantly affects the health status of the child, as this process occurs mainly in the first years of life. The nature and adequacy of nutrition, concomitant diseases, functional status herbstion tract content of fluoride in drinking water and other factors may play a role in the formation of caries-resistant or susceptible to dental hard tissues of the teeth.

Established (V.R.Okushko and snivavt., 1989) that the solubility of tooth enamel depends on the functional state of the pulp, which is associated with changes in resistance of teeth to caries. These properties of the enamel as its major strength and low solubility are provided only for maintaining high functional activity of the pulp. Mozh  cially that differences in functional status iiulpy different etagroin of temporary and permanent teeth determine the features of the development and progress of caries in children.

The functional activity of the pulp is largely related to the physical condition of the child. Chronic diseases of internal organs and body systems can lead to a decrease in the functional activity of the pulp, thereby increasing susceptibility to caries and enamel causing aggressiveness of its course.

Saliva creates an environment in which the teeth after eruption are constant.

Saliva performs many functions: it is involved in the processes of self-moochyschennya mouth and teeth has a buffer capacity, itso helps to normalize the pH in the mouth when you reduce it, is supersaturated solution on the content of calcium and phosphorus, as well as a source of receipt of these and other ions to the enamel, ensuring processes of mineralization and remineralization.

Stability of dental caries is directly related to the composition and properties of saliva. Individuals susceptible to tooth decay, the decrease rate of saliva, variations in mineral composition and reduction of antibacterial properties. Similar changes are found in the saliva of pathological conditions, minors notsinnomu food and otherwise, when the teeth are exposed to intense shock syvnomu caries.

Pathogenesis

Local factors kariesogennoy

The direct damaging effect on hard tissues of the teeth have a local kariesogennoy factors. Most kariesogennoy value (either alone or in combination with other factors) have dental plaque: plaque and dental plaque.

Plaque – a yellowish or grayish-white soft gummy deposits on the tooth surface, which is a conglomerate of microorganisms, desquamated epithelial cells, leukocytes, a mixture of saliva proteins and lipids with slices of food. Soft plaque is not constant internal structure inherent in dental plaque, it is loosely attached to the tooth surface, so it can be washed off easily enough running water or remove with a cotton ball. Dental plaque is a soft amorphous granular deposition, which is very tightly attached to the tooth surface, from which the plaque can be separated only by mechanical cleaning instrument or a toothbrush. When dental plaque is small, it is not noticeable (if not painted food pigments or dyes) in case of increasing size, it becomes gray or yellow-gray mass on the surface of the tooth.

In the attachment of dental plaque to the tooth surface is of great importance pelikula.

It is formed after the eruption of the tooth, as it is called acquired cuticle. Pelikula is a fine film that is derived protein-carbohydrate complexes saliva – mucin, glycoproteins, sialoproteyiniv (SD Hogg, I. Lightfoot, 1988). It includes three layers: surface and 2 attached quite firmly to the surface of the enamel. It is believed that pelikula is a kind of connective substance between dental plaque and surface enamel. Prerequisite formation of plaque and dental plaque is the presence of microorganisms. It has been experimentally shown that in animals hnotobiontiv (grown in special conditions of the animal, the body which no bacteria) never formed plaque and plaque. Numerous experimental studies it was found that the formation of dental plaque can be divided into several stages (IL Hardwick, 1985).

And the stage. Formation of cell-free organic film on the surface of the tooth enamel, which is called pelikuloyu or acquired cuticle. Of course it is necessary for the formation pelikuly from several minutes to several hours.

Second stage. On the surface adsorption of proteins occurs pelikuly microorganisms and epithelial cells. They stick to pelikuly gradually started growing bacterial colonies. On average, this stage lasts a few days.

III stage – the creation and formation of mature dental plaque. It happens Precipitation extracellular polysaccharides formed by microorganisms from plaque glycoproteins of saliva. At this stage, the plaque is the greatest threat to tooth enamel as actively secretes organic acids (lactic, acetic, etc..) And hydrolytic enzymes (proteases, hyaluronidase, etc..). Plaque formation begins with the accession of a monolayer of bacteria to the acquired pelikuly or tooth surface. Dental plaque is composed primarily of microorganisms (70%) and extracellular matrix (complex glycosaminoglycans and proteins). If the conditions of dental plaque increases rapidly and reaches a maximum of about 30 days.

Mature dental plaque often has the following structure (Figure.):

1. Acquired pelikula, which provides a link with enamel plaque;

2. Palisadnykopodibno located fibrous layer of microorganisms that settle on pelikuli;

3. Dense fibrous mesh of microorganisms, which are colonies of other types of bacteria;

4. surface layer of microorganisms kokopodibnyh (Z. Broucal, J. Svejda, 1973).

Scheme of the structure nad’yasennoyi dental plaque:

1 – pelikula;

2 – palisadnykopodibno are microorganisms;

C – fiber microorganisms;

4 – coca;

5 – tooth enamel

G.H. Bowden (1985) divides dental plaque microorganisms into 2 groups:

1. Acidophilic bacteria that are able to grow in an acidic environment and ferment acid;

2. Proteolytic bacteria produce proteases.

The first group includes lactic streptococci, lactobacilli, actinomycetes, leptotryhiyi and Corynebacterium. The second group are anaerobes that processed food proteins and amino acids. More important is the separation of microorganisms in dental plaque:

1. Kyslototvorni – ferment carbohydrates to form acids;

2. Microorganisms that ferment carbohydrates to form polysaccharides: dextran, Levante, etc.

The latter form network structure of dental plaque. Up to 50% of the bacterial flora of plaque streptococci constitute acidophilus dominated Str. Mutans and Str. sanguis (II Oleinik et al., 1983, 1986). On the number of species and the number of bacteria affects the availability of substrates in the mouth of food (carbohydrates, amino acids, etc..). For example, in the case of food that contains a lot of sucrose, the number of dental plaque and prevail acidophilus streptococcus.

The main proteolytic bacteria are rystely, which account for over 30% of this group of microorganisms. Important role in the formation of dental plaque play carbohydrates. Established in patients who consume a lot of carbohydrates from food (especially sucrose), dental plaque formed relatively quickly and in large quantities.

Numerous studies have shown that plaque accumulation resulting in him microorganisms able to quickly and easily convert carbohydrates into acids (lactic, acetic, propionic). Acid formation in plaque (plaque) and decreased with pH occurs only in the presence of oral carbohydrates. The easiest way plaque bacteria ferment sucrose, glucose and fructose.

Cellular elements plaque with adhesive protein telementamy ensure its porous structure that is able to pass through a oral fluid (saliva, liquid food). Formed by microorganisms extracellular polysaccharide intercellular spaces in close plaque than contribute to the accumulation of organic acids in it. Thus, plaque and especially dental plaque is a semipermeable membrane that can selectively skip through a variety of substances. Quite easily diffuse into dental plaque carbohydrates that are found there in quantities directly proportional to their concentration in saliva and exposure time. Simultaneously plaque does not pass a saliva alkaline substances that are able to neutralize the acid. Mucoid plaque film is insoluble in many chemicals. In the absence of carbohydrates plaque pH generally ranges from close to neutral – 7.0. The consumption of carbohydrates causes a sharp increase in the acidity of plaque, which lasts about 30 minutes, reaching a pH of 5.8 – 4.5. After this acidic environment is neutralized plaque buffer systems saliva pH is neutral over its values. If carbohydrate intake is repeated, there is a fairly steady decline in pH during dental plaque, causing damage to the enamel. Dissolution of enamel begins when the pH drops to 5.5, so this pH deem critical. When plaque may be a significant increase in acidity. In addition, plaque prevents the penetration of the enamel to saliva alkaline compounds that are able to neutralize acids, and inorganic substances that are constantly coming with saliva in the enamel, restoring its mineral structure.

Thus, under appropriate conditions under dental plaque may form and long maintained a condition where the concentration of organic acids will dissolve the enamel mineral structure, proteolytic enzymes and microbial plaque – split its organic components. The state of the reaction medium during dental plaque and is also influenced by factors such as age, plaque localization (by contact or vestibular surface of the tooth), the presence and concentration of carbohydrates in the mouth, the ability of carbohydrates to diffusion in plaque, saliva buffer capacity. That dental plaque largely gives the functional balance between hard tissues (enamel) and oral, because there is considerable kariesogennoy factor. Dental plaque is liable to cause a variety of immunological reactions. Proved that it contains immunoglobulin A, G, M, amylase, lysozyme, albumin and other protein substrates. Immunofluorescence methods were found to be harboring immunoglobulin tooth plaque and bacteria. For example, bacteria coated with IgA, coming from saliva or gingival fluid (GD Ovruchskyi, VK Leont’ev, 1986; Wiltont IM et al., 1988). This immunoglobulin is the main factor that prevents the adhesion of microorganisms to the surface of the dental hard tissues (enamel) and the formation of their colonies. Given the significant role of antibodies in the development of many pathological processes have attempted to link to their caries reduction or absence (especially IgA) in saliva. However, the findings are inconsistent, since it is difficult to link the general secretory antibody multifaceted system only with local manifestations in the oral cavity.

Soft dental plaque are quite pronounced enzymatic activity. Total number of enzymes found in dental plaque and dental plaque, more than 50, most of them are of microbial origin and are proteolytic enzymes. Besides them there phosphatase, neyraminaza, lactate dehydrogenase and other glycolytic enzymes of glucose degradation pathways. Under the action of microorganisms and enzymes of glucose and sucrose undergo enzymatic transformation. First, sucrose is converted to polysaccharides such as dextran and Levante who are reserved, and then hydrolyzed to glucose and fructose. Later they also phosphorylated by glycolytic converted to pyruvate. Further pyruvate can be reduced to lactate (lactic acid) by the enzyme lactate dehydrogenase, dekarboksylyuvaty in acetate (acetic acid) under the action of pyruvate decarboxylase or included in ttsykl Citric acid and form a number of organic acids, including succinic. Last under the influence of specific enzymes is converted to propionate. The combination of these acids (lactic, acetic, propionic) and forms a common set of dental plaque acid products that damage the mineral component of enamel. Among the predominantly lactic acid, which is produced mainly streptococci. Perhaps kariesogennoy properties of dental plaque is associated with it, because lactic acid has the ability to dissolve calcium apatite teeth even at pH above the critical value.

Role of microorganisms in caries development

The significant role of microorganisms in caries was confirmed by another work W. Miller, which enabled him in 1884 to formulate a chemical-parasitic theory of caries. Numerous subsequent studies has been very carefully studied microflora cavity and mouth, which allowed her to make a clear role in causing tooth decay.

Microbiological studies since the mid-XIX century., The cavity was discovered quite varied and numerous microflora. On the basis of the properties of its individual species, their prevalence in people with cavities and without their presence was revealed some relationship between different groups of microorganisms and caries. First it was the bacteria that can exist in an acidic environment and ferment carbohydrates, turning them into organic acids (called acidophilus and atsydohenni bacteria). Often these were some strains of streptococci, to a lesser extent – representatives of other species – lactobacilli, actinomycetes. The ability to ferment carbohydrates to form organic acids (lactic, acetic, propionic) is the most characteristic feature kariesogennoy microorganisms.

Streptococci of the cavity were first isolated in 1900 p., Was later found their quantitative predominance (50%) of all isolates kariesogennoy microorganisms. Assumptions about the important role of streptococci in the development of dental caries based on their quantitative predominance of the cavity, enzymatic characteristics, to identify them more than 50% of dental plaque and at different stages of caries lesions. According G.H. Bowden (1985), streptococci constitute 70% of the colonies, and veylonely neyseriyi – 15%, other microflora (dyfteroyidy, lactobacilli and other.) — 15 %.

Experimental conditions were simulated oral in vitro in the chemostat (so-called artificial mouth), which studied the peculiarities of growth and kariesogennoy of some microorganisms. The ability to cause demineralization of teeth has been established only in some species atsydohennyh microorganisms, for example, the strongest it has been in Str. mutans. Convincing experiments to prove the role of microorganisms in the development of caries were conducted F. Orland and colleagues (1964) Animal-hnotobiontah. It was found that in these sterile animals, even though they were on kariesogennoy diet (diet with a predominance of carbohydrate), caries not occurred. At the same time, the control group of animals that were ion-sterile conditions on the same diet, almost 100% of cases occurred caries. To clarify kariesogennoy activity of certain types of microorganisms, one strain was administered to food animals hnotobiontam (called monoinfikuvannya when the animal is only one type of bacteria). As it turned out, most types of microorganisms isolated from the oral cavity, causing no tooth decay, except kyslototvornyh bacteria (streptococci, lactobacilli and some others). Kariesogennoy highest activity in these animals was found monoinfikovanyh when entering streptococci, especially strain Str. mutans. This strain causes the most rapid development of caries with many (75%) of the affected teeth. Nowadays, the properties of this strain of streptococcus studied in great detail and shown its crucial role in the occurrence of dental caries.

Str. mutans often detected on the surface of the enamel, where it is a large proportion of the microflora of dental plaque. It prevails among organisms and materials from pits, fissures enamel interdental spaces, places that most often localization of caries. Very important is the fact that Str. Mutans normally absent from undamaged enamel surface if there is no plaque. There have been many studies that have established the prevalence of caries indices correlation with the presence of Str. mutans in the oral cavity. It was also demonstrated the ability of Str. mutans to adhere to the tooth surface by their synthesis of extracellular polymers such as dextran. It should be noted that other types of microorganisms can synthesize kariesogennoy of carbohydrates (especially from sucrose) vysokopolimerni glucans (dextrans, Levante), hyaluronic acid. These polymers enable the bacteria to adhere to kariesogennoy hard tissues of teeth (the enamel) and form the matrix of dental plaque.

In the experiment on animals P. Keye (1962) found that streptococci producing dextran, have a higher kariesogennoy activity. Such specific to Str. mutans properties, but less pronounced, with other strains of streptococci kariesogennoy (eg, Str. sanguis, Str. salivarius, Str. mulleri and some others). In the cavity and saliva of patients with dental caries bull found a significant number of lactobacilli. In the experiment had proved their high atsydohennist, atsydofilnist and ability to cause damage to the enamel kariyesopodibni. People with active caries process flow revealed a higher content of lactobacilli in saliva than healthy. Based on the determination of the number of bacilli in kyslototvornyh saliva test has been developed so-called laktobatsylyarnoho number, which can be an indicator of the activity of the caries process, or predisposition to the development of caries. Although lactobacilli are so active properties caot be considered the main microbial agent of dental caries.

Animal experiments, hnotobiontah been proven that kariesogennoy activity have only a few strains of lactobacilli (Lactobacillus acidophilus, Lactobacillus casei). It also established a major role in the destruction of lactobacilli dentine caries process. As you know, streptococci constitute almost half of all dental plaque microflora, lactobacilli – only 1%. Isolated from cavity streptococci have the ability to reproduce the experiment quickly, within a day after cultivation, they cause a sharp increase during plaque acidity – pH to 3.4. Lactobacilli reach a pH just 3 – 4 days, but so few of them able to give a very significant effect kariesogennoy. Assumptions about the possible role of other microorganisms in carious lesions of mainly based on the fact that many members of the oral cavity with active acidophilus and theoretically can cause demineralization of enamel. This assumption is evidenced by the fact polimikrobnosti dental plaque. Some of these species are resident microflora can cause caries in animals hnotobiontiv, but their role in the development of dental caries in humans has not been sufficiently clarified.

The scheme of the pathogenesis of dental caries

Scheme participation of dental plaque microorganisms in the pathogenesis of dental caries

classification.

 In pediatric dentistry posluhovuyutsya common classification of caries lesions characterizing ¬ ing teeth nature of the flow, depth and localization.

I. Localization: fisurnyy (caries fissuralis); aproksymalnyy

(caries aproxsimalis); cervical (caries cervicalis); combined

location (buccal, labial, tongue surfaces).

ocalization of cavities:

A – fisurnyy, B – tooth contact surfaces (aproksymalnyy);

B – cervical, G – circular

 

II. For deep lesions: initial (caries incipiens); over ¬ Neva (caries superficialis); median (caries media); deep (caries profunda).

 

III. The nature of the clinical course of acute (caries acuta);

chronic (caries chronica).

chematic representation of the cavity when

acute (A) and chronic (B) of the disease

 

IV. For consistency of occurrence: primary (caries primaria); secondary or recurrent (caries secundaria, seu recidiva). Along with the characteristics of carious lesions in a sepa ¬ mo tooth taken suggested (T.F.Vynohradova, 1978) to assess the activity of the caries process in the body as a whole. The author identifies three degrees of disease activity:

 And – compensated cavities;

II – subcompensated,

 III – decompensated (табл. 21).

The distribution of children into groups according to the degree of activity of the caries process is essential in organizing dental care pediatric population, particularly during sanation and preventive measures.

 

Table 21. Assessment of intensity of the caries process (with T. Vinogradova, 1978)

Age of child,   years	Performance intensity decay depending on the degree of activity
	І — – offset   form (CPV + kn)	II — subcompensated form (CPV + kn)	III — decompensated form (CPV + kn)
7-10	Up to 5 teeth	Up to 4 teeth	Up to 6 teeth
11-14	6-8 teeth	5-8 teeth	7-9 teeth
15-18	More than 8 teeth	More than 8 teeth	More than 9 teeth

 

hat the depth of caries in children is the notional value, which depends not only on the size of the cavity, but also on the volume’s fixed camera. What is a “junior” tooth, the more volume it’s fixed camera and the in ¬ pared deeper cavities are.

Figure 28. Cross-section of the center of the initial caries (saL. M. Silverstone, 1981).

and – the surface layer, b-body lesions, in – dark zone; / – area hipermi-neralizovanoyi enamel.

And – look at polarizing microscope, B – schematic representation pas tomorfolohichnyh zones in enamel.

Pathological morphology of dental caries . Under a bright spot or initial caries with polarization microscopy detected cell lesions of enamel in the form of a triangle , whose base povernenado outer enamel surface ( SM Studevant, 1995, fig. 28). There are four zones: 1st – surface area, 2nd – body injury, 3rd – dark zone , 4th – transparent area.

The transparent zone is deepest . This area hipermineralizo – Vano enamel. It pores and voids located along the enamel prisms . Pore ​​volume in the clear zone of 1% , which is 10 times higher than in intact enamel.

The dark area is called so because they do not transmit polarized light will not ¬ . It has a large number of tiny mikroprostoriv under ¬ povnenyh air or gaseous substances that cause absorption with polarized light. Pore ​​volume in a dark area amounted ¬ vyt 2 to 4%. There is loss of the crystal structure of enamel. The width of the dark zone depends on the intensity of reminera – ation , while it may increase.

Body defeat – the largest volume area with obvious signs of de- mineralization. Pore ​​volume of from 5 % to 25% of the periphery to the center area. It can mistytytys bacteria, so that the size mikropros ¬ tors in the enamel enough to penetrate deep into them . Dissolution of enamel occurs along the lines Rechtsiusa as spaces along them relatively little mineralized .

Surface area hardly affected by caries . Pore ​​volume in ¬ it is not great compared with body damage ( meiishe U / O ) and mikrorenthe – tech is not different from the intact enamel.

The surface of intact enamel hipermineralizovana because of pos ¬ of continuous contact with the saliva , and the high content of fluoride ion in over ¬ Nebo layer of enamel making it more resistant to caries damaged ¬ tion versus located deeper layers. However prohresuvan ¬ ing caries process leads to the formation of the surface layer of enamel conical defects through which bacteria can enter inside the enamel.

Numerous electron microscopic study of enamel at different stages of carious spots revealed disorientation crystal ¬ sustainable hydroxyapatite , change their shape and size , the formation of atypical ¬ ing for normal enamel crystals.

At initial caries observed changes in the dental pulp : disruption of odontoblasts layer , change their shoots and homohe ¬ tion of the cytoplasm and fatty degeneration of connective tissue cells and extracellular material changes pulp.

At the surface and the average caries detected destructive ¬ tive and reactive changes of enamel and dentin.

Enamel- dentine combination of the least resistant to carious lesions, tooth decay because this place is spreading rapidly and carious lesion in dentin has a V- like shape with the apex directed toward ¬ tion pulp ( SM Studevant, 1995, fig. 29). This may explain the rapid spread ¬ You caries in teeth in children by plane (called the plane caries of deciduous teeth).

Pulp – dentinal complex responds to carious lesions intensification of mineralization of dentin to block dentinal tubules. This reaction is a result of enhancement of functional acciency odontoblasts in response to the demineralization process . Rose  riznyayut 3 types of responses to dentine caries process : 1) a reaction to a long, slow process of progressive low- acid demineralization lotnoyi 2) response to moderate- intensive process ;

3) reaction to the active, rapidly progressive carious process with high levels of acid demineralization

Chart. 29. Schematic representation of the occlusal surface caries (for SM Studevant, 1995). The enamel on the chewing surface appears to be intact, as carious cavity has an inlet point in fissures. In ca-riozniy cavity contains a large number of streptococci and lactobacilli. The upper layers of dentin infected them. The lower layers of dentin is not yet infected, but much of demineralized. Substitution (reparative) dentin begins to form under the damage area

The determining factor in the implementation of protective changes in dentin with pulp zhythyezdatna with sufficient blood circulation and microcirculation .

In case of slow progress of caries pulp can restore demineralized dentin by dentin remineralization intertubulyarnoho . Dentin , which contains more mineral substances ¬ wines compared with intact called sklerozovanym . It is an obstacle to deepening the caries process , because it dentinal tubules almost completely blocked.

The second type of response is determined by a moderate dentin caries progression process. In the dentin contains a large number of pathogenic factors such as microorganisms,  ucts of their life, hydrolytic enzymes , remnants ¬ cial bacterial cells that can lead to degeneration and death of odontoblasts and their processes in the affected area and cause irritation of the pulp. Battered dentinal tubules forming the so-called dead path in dentin . In the pulp under the influence of substances coming through these ways of dentine formed secondary or so-called substitute Odon – toblasty (from undifferentiated mesenchymal cells). These cells produce reparative  HN (reactive ) dentin from carious pulp according to cell ( Fig. ZO ). This differs from secondary dentin dentin producing odontoblasts his Pul ¬ pi for life. Often the structure of reparative den portion irehulyarna and amorphous . Dentinal tubules there are no particular orientation .

The third type of response dentin detected in acute , progressive velocity com ¬ caries with high levels of acid . If the strength of destructive factors greatly exceed the protective capabilities of dentin and pulp, in which case the inevitable happens infection and inflammation of the pulp.

In carious tooth dentin distinguish 5 zones patomorfolohich -tion changes more clearly reveal the slow progress  bathroom decay, ie with its chronic course.

The first zone is the deepest – a zone of normal dentynu.U it is dentinal tubules with spikes odontoblasts , no crystals in tubules and bacteria.

Chart. 3O . Schematic representation of intact dentin caries (for SM Studevant, 1995).

A. – intact dentin :

and – prypulpovyy dentin is characterized by extensive dentyynymy Canal tsami , lack perytubulyarnoho dentin mineralization weak inter- tubular dentin ;

b – in dentin layers located farther from the pulp dentynpi narrower tubules , they are surrounded by perytubulyarnym dentin , dentin intertubu her regular uniformly mineralized .

B – carious dentin :

1 – zone of normal dentin , which is located near the pulp. Characters ¬ zuyetsya some narrowing of dentinal tubules due process hipermi – neralizatsiyi ;

2 – zone of carious dentin damaged . It is characterized by loss of minerals and intertubulyarnym perytubulyarnym dentin . But there are no bacteria . The accumulation of crystals of minerals occurs in the lumen of the dentinal tubules. This area of dentin transparent ;

3 – zone of carious dentin infected.

 It is characterized by a large number of microorganisms in the dentinal tubules and destruction of organic structures dentin.              

The second zone – translucent dentine . This area demsheralizatsp intertubulyarnoho dentin and early formation of very thin crystalline ¬ hoists in the lumen of the tubules Significant damage processes odonto – blasts , but no bacteria in the tubules .

The third zone – transparent dentin. This layer of dentin characterszuyetsya further loss of minerals intertubulyarnym dentin and deposition of large crystals in the lumen of the tubules. It is softer compared to intact dentin . The bacteria do not. ¬ collagen fibers remain in the new structure as possible samovidnov -tion of the dentin in the living pulp.

The fourth zone – a zone of dentin with impaired histological structure. Characterizes hsya expansion and distortion dentin tubules ¬ them that are filled with a large number of microorganisms. There are very few minerals and collagen fibers destroyed.

The fifth zone – infected childr forth. This area was destroyed dent so steeped in lots of bacteria. The structure of dentin is not defined because there are no minerals and collagen fibers .

With an average caries are changing in the pulp. Odontoblasts layer thinned, vakuolizovanyy . Under the electron microen masse in odontoblasts revealed increased mitohondrp and weak korozvynena endoplasmic reticulum .

With deep caries , especially if it is an acute course, vidsuhni transparent zone ( sklerozovanoho ) zone intact dentin and dentin. Dentin bottom cavity substantially demineralized with varying degrees of degenerative changes in organic matter The reducnd in the pulp revealed significant changes bahahma authors lo ¬ tozhnyuyutsya initial phases of inflammation ( redness pulp).

 

Symptoms, diagnosis and differential diagnosis of caries of deciduous teeth

Clinic. Children of all ages caries has some features of the course. Anatomical and histological features of the structure of deciduous teeth, morphology and functional activity of the pulp at different stages of their development, and the general condition of the child’s body reactivity of an impact on the progress of caries. The clinical ob ¬ conservation suggests that the progress of caries in temporary teeth closely associated with the stage of development of the tooth.

 

Caries of deciduous teeth at the stage of root

A prerequisite for the development of early caries of deciduous teeth in children 1-3 years is disturbance of structure formation of hard tissues of deciduous teeth. It could be due to chronic somatic diseases are the mother before pregnancy, severe metabolic disorders in the mother during pregnancy (talk  sycosis 1st and 2nd half). Early lesions of teeth and their rapid Ruinuvannya often seen in premature infants, as well as those who are ill in the first months of life, and other infectious diseases (rickets, indigestion).

Feature of clinical caries of deciduous teeth in step form ¬ ing root is extremely sharp and acute course. Carious cheer ¬ tion localized mainly in the cervical area of ​​the upper incisors and the furrows of the first and second temporary molars. Tooth decay progresses rapidly , spreading on a plane and cover are resistant to decay in ¬ upper teeth ( incisors in vestibular , bumps in molars ). Vidznachayet ¬ be as rapid destruction of temporary tooth dentin because of its weak mineralization and lack of defensive reactions from mor ¬ folohichno and functionally immature pulp.

A characteristic feature of early caries lesions is the multiplicity of deciduous teeth and symmetrical arrangement of carious defects.

Despite the progress of active caries process , it is usually not accompanied by subjective feelings . This greatly complicates the differential diagnosis of various stages of decay between themselves and its complications , which most often manifested in the case of multiple disease.

Caries of deciduous teeth at the stage of root charac ¬ ryzuyetsya rapid transition in uncomplicated complicated. This is due to anatomical features of the structure of dentin and pulp in temporary teeth during this period : wide dentinal channel, a thin layer of mineralized dentin enough of pulp , a significant volume of the cavity of the tooth, the pulp horns that are close to the enamel- dentinal connections. Morphologically and functionally immature Pul ¬ pa at the stage of temporary tooth caot form sklerozovanyy (clear) and substitution ( reparative ) dentin that hinder the progression of the caries process .

In front of the upper jaw teeth are temporary and sometimes in molars caries can begin in the cervical area. Later, he distributed circular , covering the whole tooth. This form ca ¬ riyesu was called circular . Starting at anywhere near the neck of the tooth , often in the form kreydopodibnoyi spots fast decay com ¬ spans the neck, and then all temporary tooth crown . Ur ¬ tion of hard tissue is quite shallow , but quickly spread across the plane, all enamel layer existing disease that is easily broken. For ¬ Primary localization of the process observed mainly on the labial surface, in some cases – in language . The process can restrict ¬ tysya one temporary tooth surface , but quite often it spread ¬ ryuyetsya aproksymalni on the surface , leading to co- cast Ronco tooth. In the jaw , leaving only the roots of deciduous teeth , pulp flow in such cavities are usually nekrotyzuyetsya . ¬ Not rarely this age parents bring to the dentist when periodontitis has emerged in the area of ​​the front teeth of the upper jaw with porytsyamy on the gums, oozing pus or granulation of them ( see Figure 6 – see . Colored inset) .

Dental temporary molars in young children (2-3 years ) is characterized by acute course , is localized in the furrow and is intended to encompass beyond the enamel- dentinal connections , ie the depth of affection ¬ tion prevails medium and deep cavities. Carious cavity ¬ Nina light edge enamel thinned easily break off , dentin karioz ¬ tion cavity light, moisture, removable layers, and the whole process does not tend to limit.

 

Caries of deciduous teeth formed at the stage of root

Acute initial caries – a transient stage of caries of deciduous teeth , so the hospital is rarely diagnosed . Carious spots are located in areas of typical localization of caries, ie fisu – Rahim , the aproksymalpyh surfaces of incisors and molars and in the cervical area. However, clinically carious spots often appear on the vestibular surface of the incisors temporary because these areas itso well foreseeable . Carious spot , usually covered with a thick layer of plaque, no subjective data , objective – while removing plaque and drying the surface area visible white enamel ¬ of color, which have lost their natural luster. Acute primary tooth can become chronic course or go into sharp ¬ ing surface caries.

Superficial caries is more acute course and with the consequence of ¬ strictly initial caries. Burying caries in enamel ¬ nated accompanied by the appearance of carious defect, but that does not cross the enamel- dentinal connections. Localization of acute superficial ¬ carious cavities corresponding to the localization of spots. Defects of enamel ext re ¬ visible on clinical examination and have the appearance of areas Cray – dopodibno modified enamel with visible destruction of its structure. When probing determined rough , softened surface. Complaints are usually absent. Older children may complain of the action of chemical stimuli ( sour, sweet).

Chronic superficial caries of deciduous teeth on the stage of formation of roots is rare. There is a lack of subjective sensations. It appears during the clinical examination of the child. Carious defect looks like a dark brown plya ¬ we defective enamel sensing does not cause painful sensations.

Average caries . Acute secondary caries of deciduous teeth – one of the most common clinical forms cavities formed at the stage of root. The child may complain of delay of food between the teeth sensitivity ¬ lyvist in the event of chemical and thermal stimuli. Sometimes complaints can ¬ may be available. During the physical examination detected carious cavity with a narrow inlet . Pidryti edge enamel with matte white. Dentin that fills a carious cavity ¬ nynu , light yellow or yellow color , soft, removable layers for an excavator . In aproksymalniy surface caries may cover the entire surface with little depth. In raids, formation of thin edges of enamel carious cavity may have broad ¬ cue inlet . Probing bottom and sides cavity is usually painless. It should be remembered that these sensing in such cases you ¬ is not always objective , due to the psycho-emotional state of the child during treatment.

Chronic secondary caries is localized mainly in aprok – being maximum surface , at least – for chewing and cervical . The clinical course of this form of caries in temporary teeth bezsymp -volume . Complaints may be the presence of the cavity or delay food between the teeth. Cavity has a wide inlet , its walls and floor are covered with dense pigmented dentin . Areas ¬ ment walls and floor painless.

Sometimes somatic healthy children revealed significant planar defects of hard tissue (called planar cavities ) with dense, shiny, smooth in probing the dentin . They are located on the chewing surfaces of temporary molars. This condition can be regarded as suspended caries ( tooth decay stationary ). It could be due to improved overall physical health di ¬ fences and changes kariesogennoy situation in the mouth.

Deep cavities formed at the stage of temporary tooth root is more acute course. Subjectively children may complain of pain as a result of mechanical or thermal stimuli.

During the physical examination should carefully examine the causal tooth, pay attention to the intensity decay and deter ¬ cheats history of the state of general physical health of the child. Cavity hfy acute deep caries localized within prypulphyuvoho dentin. Yii depth in temporary teeth are smaller than regular , because of the anatomical and topographical features of the structure of deciduous teeth.

It should take into account the location of the cavity. When placing the cavity in aproksymalniy surface where the layer of solid fabric is quite thin and the distance to the pulp insignificant complications of caries development is faster. Because acute course of decay with a cavity on the surface aproksymalniy temporary tooth is often a sign of complicated caries .

If the active current caries in temporary teeth do not have time to be produced vicarious ( reparative ) dentin from the pulp, not pronounced protective hardening in the dentin . Dentinal channel are broad processes of odontoblasts quickly destroyed tubules filled with a mixed bacterial flora , as irreversible changes in the pulp of deciduous teeth can be observed at clinically shallow cavities. Therefore, the diagnosis of acute deep caries of deciduous teeth should be set very carefully after a thorough diagnostic differentiation tion of its complications.

Chronic deep caries in temporary teeth in children under the prevailing root does not occur often. It can be diagnosed in somatic healthy children with low intensity of the caries process . Chronic tooth decay is characterized by free ¬ progression , the formation of dense , sklerozovanoho dentin due to activation of protective function of morphologically mature pulp. Subjective complaints during the course of this decay are absent. Objectively manifested in the tooth carious cavity with a wide inlet . Carious dentin thick, is dark brown or black color -ing , excavators removed hard nry sensing probe is not retained and easily glides over the surface .

In addition to acute and chronic course of caries in temporary teeth in the clinic are so-called intermediate forms between the classical signs of acute and chronic caries. Thus the observed  yutsya moderately severe pigmentation and decalcification of dentin cavities. Dentin is the yellowish – brown color , but the texture is not hard, as in the case of chronicity.

Caries in deciduous teeth root resorption stage

At the stage of root resorption of deciduous teeth caries zustrichayet not be often. The clinic is mainly diagnosed complication of tooth decay in the form of chronic pulpitis and periodontitis. However, the soma- cally healthy children carious process in temporary teeth may have a typical chronic course. For deep affection prevails ce ¬ vious and deep cavities , rarely observed surface caries as pigmented spots, which is localized on the surface of polar vestybu temporary canines. Localization dominated aprok – being maximum caries. According to TF Vinogradova (1988 ), localization of caries on surfaces aproksymalpyh temporary molars and upper incisors observed in almost 60 % of cases, whereas in the cervical area , it is found only in 5 % of patients.

Acute course of caries of deciduous teeth on the stage of resorption comrenya rarely diagnosed and usually in children with common catfish  cal diseases and reduced immune reactivity. In this appeal no hope stimuli .

Thus , the flow of caries of deciduous teeth has certain laws ¬ nomirnosti corresponding stages of their development.

Differential diagnosis of caries of deciduous teeth. If the diagnosis of caries of deciduous teeth occurs, usually without much difficulty , the differential diagnosis of non- complicated and complicated caries of deciduous teeth – extraor ¬ but responsible and difficult task that confronts every stoma ¬ tolohom pediatrician . Age of child difficulties contacting, ¬ insufficient classification of their feelings baby occasionally make this task extremely difficult. Therefore, differential diagnosis of caries of deciduous teeth is based mainly on data from the objective circumstances -tion of the child. At the same time pay attention to the depth and location of the cavity , the color and texture of the affected dentin, espe ¬ cially condition dentin layer at the bottom of the cavity , the condition of the mucous membrane of the gums and transitional fold area carious tooth.

For differential diagnosis of caries of deciduous teeth develop m’yakshenyy dentin should completely remove an excavator or Kulas by boron. If this open cavity of the tooth within the softened dentin , the diagnosis is not difficult to figure out . The presence of Pulpi bleeding and reacts to sound , confirms asymptomatic tion of chronic fibrous pulpitis. If the probe conattraction cavity with pulp chamber painless, it may indicate a chronic gangrenous pulpitis or chronic granulating periodontitis. To confirm this , carefully inspect and palpate soft gum tissue and transitional folds in the area of ​​the affected tooth. The presence of even slight hyperemia rederivatives folds or fistula on the gums evidence of asymptomatic periodontitis temporary tooth. The final diagnosis is established  regimenting after X-ray examination.

Symptoms, diagnosis, differential diagnosis of caries of permanent teeth

Clinic. Caries in permanent teeth of children as the mass of a certain person ¬ portunities course. They are mainly associated with the stage of formation of permanent teeth and mostly – the state of health of the child that EID ¬ Nacha its immunological reactivity. The frequency lesion 1st place went to the first and second permanent molars of the lower jaw, on the 2nd place – these very teeth of the upper jaw. They were subjected to shock upper incisors and premolars . Less commonly observed lesions of the upper canines and lower premolars. Quite resistant to caries lesions lower incisors and canines .

In children, severe forms dominate the flow of permanent teeth caries is caused by the incomplete mineralization of hard tissues nin permanent teeth that have just erupted , and the hysnoyu sufficient for the function of the pulp during the completion of their formation. The less time since the eruption of the tooth to its defeat , the sharper and more rapid progress of caries. During the generated correlationtion of permanent teeth more frequently than acute , there is an intermediate and chronic caries. This is due to the stabilization of the structureri enamel and dentin and pulp of functional maturity that the ability to deter rapid spread of the caries process by making you  substitution and transparent dentin. Acute progress of caries in adolescents , covering a large number of permanent teeth, indicating the presence of immune deficiency in the body. Therefore, it is obligatory  careful examination of these children are not pediatricians ( Gastroenterologist, endokry -gies et al. , Fig. 7 – dyv.kolorovu inset).

 

 

Localization of carious lesions is also associated with stage forming tooth. In teeth with immature root caries locale  zuyetsya mainly iatural cavities and furrows crownsing . Furrows – enamel cover this area , formed by the merger of molars or premolars hills that form  Xia and mineralizuyutsya separately. Some pieces of landing tooth crowns that are saturated with mineral salts, increasing merge and form a single occlusal surface of the tooth . In places of connection and form furrows , folds and holes. Thicker enamel cover at the junction of some relatively small hills and bottom grooves separated from the dentin to priorities would need a thin layer of enamel ( 0.5-0.6 mm). At the time of tooth eruption in a child furrows are less mineralized areas we crown. Retention of food in the furrows, which are directed at nesfor – tooth deep and wide, resulting in early cheer  tion of caries (Fig. 31). During the formation of roots  localization of caries in the furrows observed much less frequently , giving aproksymalnomu location in carious cavities in permanent teeth of all groups.

 

Chart. 31. Caries development in the area of ​​fissures (polarization microscopy).

A – tooth decay begins in the region of the inlet in the fissures and localized

only within the enamel of the arrow.

B – due to lesions of enamel fissure caries at the bottom of the process extends to the dentin

As for the depth of the lesion , the permanent teeth in children can identify all forms of dental caries : initial , superficial , medium and deep ¬ Bokij . However, the clinic is dominated by medium and deep cavities.

Initial caries or carious enamel demineralization (caries incipiens, seu macula cariosa), clinically characterized by a change of co ¬ loru in a limited area of enamel – the appearance of spots. Children of glass ma ¬ often has a white matte , less brown or black ¬ ing . In the initial stage can often diagnose caries on the exposed surfaces of teeth – vestibular and cervical . So if you start talking about tooth decay, or cavities in stage spot, ¬ tion should mean caries vestibular surfaces of front teeth or cervical surface of all the other teeth. It should be borne in mind that each cavity regardless of its location must re ¬ blowing an early stage in the form of patches.

Spot white larger than 1 mm would take ( H.N.Pahomov , 1974) for the first clinical stage of decay. Increasing the size of spots is accompanied not only by an increase in the area of enamel lesions , but also the degree of destructive patomorfolohich – change.

When gaps larger than 3 mm of the pathological process ¬ fully covered layer of enamel , causing changes in the enamel- den combination hospitable and even in dentin . Changes of organic matter in ¬ shkodzhenoyi zone material .

Brown spots are fundamentally different from whites ¬ we greatly destructive changes in organic matter of enamel. When you ¬ roof of hard tissue lesions always drawn into the process of enamel- dentine connection and turns reaction ( sclerosis) of dentin bordering the center of the pathological process. The depth of the lesion responsible Square ¬ charge spots.

Acute initial caries in children are usually not complaints. His doctor finds during the examination of the teeth. Plot naychas ¬ lesions more often covered with plaque removal after which exhibit piece white enamel that have lost their natural luster. Returning ¬ hnya enamel is smooth , sometimes a little rough , but painless and very hard. In permanent teeth kreydopodibni spots detected in the cervical area incisors and first permanent molars , and in children 12-15 years – in the area of the necks of the canines, premolars , molars less .

Acute initial caries is diagnosed more often in children with III degree of activity of the process , which includes a large number of teeth, INCO ¬ ly even all teeth. This may indicate a significant shift in a state of systemic and local immunity of the oral cavity, which ob ¬ rihayutsya chronic diseases of internal organs and body systems.

Diagnosis of acute initial caries carried out first of all ¬ ed visually. To do this, clean the enamel surface of teeth on the fly ¬ thoroughly dried air stream. The affected area becomes opaque enamel shade resembling enamel after mordants state ¬ ment when working with composites .

For the differential diagnosis of acute initial caries lesions from non-carious hard tissues ( enamel hypoplasia , flyuo develop ¬ ) is most often used method zazhyttyevoho (living ) in ¬ staining with 2 % aqueous solution of methylene blue ¬ nd . For this enamel surface previously cleaned, treated with hydrogen peroxide and dried. Teeth are isolated from saliva and put them in the dye solution for 2-3 minutes. Then dye wash water stream. Damaged areas of enamel in acute initial caries ¬ tural , unlike hypoplasia and fluorosis , stained with varying intensity. Assess the color on a 10- point scale. As the dye can be used as 0.1 % aqueous solution of Me ¬ tylenovoho red.

The method of electrometric diagnosis of caries and com ¬ plex devices to detect initial caries not only on the types ¬ IIR sections of the tooth , but also in the furrows ( V.K.Leontyev , 1983). Method of soil ¬ tuyetsya the ability carious tissues conduct electrical current of varying size depending on the degree of injury.

In addition, in order to diagnose the initial decay can be per- stosovuvaty method stomatoskopy ‘ ultraviolet irradiation, based on the effect of luminescence hard tissues : healthy tissue lyuminestsiyuyut light green. Dental promotes ¬ Sonny luminescence of said hard tissue . It is larger, the deeper the pathological changes in the structure of the enamel.

Recently stomatoskopichnoyi for diagnosis of caries using fotopolimeryzatory that they are used to working with composite photopolymer materials .

Differential diagnosis of acute initial caries of enamel hypo ¬ plaziyeyu (especially thistle shape) and fluorosis are in tabl.22 .

It is extremely difficult to differentiate acute initial caries fisurnyy permanent teeth , and insufficient mineralization fissures of premolars and molars. The basic clinical research method – probe ¬ tion – does not show significant differences , as demineralized enamel and poorly mineralized equally tempered and rough during probing.

During the formation of roots of permanent teeth grooves naychas ¬ more often pigmented , so a correct assessment of mineralization and diag ¬ teak initial caries – important task for dental  ha pediatrician . It should be borne in mind that most of them mineralizova fissures , even in the presence of the pigment should not be regarded as an initial or superficial caries, as mineralized as connector may be resistant to decay during the whole functioning of the toothtion . Pigmented groove in which the probe is not delayed nor deepens, should not be considered as initial caries. In furrows  priorities would need to see a stabilization of caries often requires no plom  accommodated.

Table 22. Differential diagnostic signs of acute initial caries, enamel hypoplasia and fluorosis

 

Superficial caries in permanent teeth of children occur in place of white or pigmented spots due to progression of destructive changes in the enamel. Characterized by the softening of the affected enamel is removed with little effort excavator. Most children at this stage of the pathological process any complaints are observed. Some of them complain of intermittent pain from chemical irritation ers – sweet, salty, sour.

If in the case of excavation stripped enamel dentine is destroyed enamel- dentine combination , then the tooth should be considered for this vious .

Clinically surface caries is under examination in upper tooth ( enamel discoloration ) and during probe : sharply expressed weighted roughness, probe delay , defects of enamel.

Differential diagnosis of acute superficial caries should be conducted with acute primary and secondary caries, alveolar form of systemic or local enamel hypoplasia , as well as erosive form of dental fluorosis. Hot surface caries differ from the initial acute complete destruction of the surface layer and Society ¬ lyblennyam pathological process in the enamel. Unlike acute , intermediate decay is characterized by a sharp surface retentiontion intact enamel- dentinal combination that at the average caries always destroyed. With an average caries cavity commonly lyblyuyetsya to dentin, enamel- dentinal sensing communication in case of acute flow causes pain.

Cellular form of enamel hypoplasia differs from the initial decay multiplicity of defects and symmetry of their location. No signs of hyperesthesia observed. Hypoplastic defect charac teryzuyetsya correct spherical contours, edges are smooth out  Eugene. The bottom of the defect is always smooth and shiny .

Local hypoplastic enamel (tooth Turner ) , as opposed to surface caries, enamel defect characterized by irregular shap we often pigmented , located on the mound pre- molars or on the cutting edge of front teeth . The bottom of the de defects formed by a thin layer of enamel or dentin sklerozovanoho . This non-carious lesions of teeth relatively early caries complicated .

Erosive form of endemic fluorosis as surface caries is characterized by a defect within the enamel. However, when defluorosis enamel defects can be located on any surface of the tooth, including resistant to decay. Caries process in such defects is practically not observed. Since erosive form of fluorosis occurs when the use of drinking water with high fluoride content (in mg / l or more ), the signs of fluorosis manifest in the majority of children who live in the region.

Average caries of permanent teeth in children diagnosed naychastist . For this form of caries process violated the integrity of the enamel- dentinal connections, but on pulp chamber remains unchanged fairly thick layer of dentin. In most children , this forma permanent teeth caries complaint is not so diagnosed, usually in the rehabilitation of the mouth or teeth review of medrem dentist.

Cavity is characterized by a small input from vorom . Occasionally affected furrow comes only probe that there is attrymuyetsya . The edges of the enamel that covers the entrance to the cavity, can be kreydopodibno changed, especially in the in aproksymalnyh upper front teeth. Therefore, to determine the depth of the lesion den  portion , and thus tooth decay and form is possible only after preparuvaning cavity , which is a sensitive (if performed without anesthesia ) through stimulation enamel- dentinal  combinations of boron.

For older children who are healthy somatic , in the teeth of the external check vanym root caries diagnosed chronic middle . The character  it for it is a slow progression in dentin walls and bottom carioznoyi cavity rather dense, brown. As a rule ¬ lo , these children are diagnosed form of activity offset carioznoho process.

Differential diagnosis . Average caries of permanent teeth in children should be differentiated primarily with deep caries , as well as chronic peryudontytom . During the differentiation state trough medium and deep cavities should pay attention to the depth of the cavity after preparation. It should take into account  wool in permanent teeth with immature root pulp relatively larger volume because carious cavity at a relatively lower its depth can be located close to the pulp. Acute invincibly  cue caries tooth is more sensitive to thermal and mechanical stimuli. Cool in the tooth affected by acute deep caries  bokym , there is pain that passes quickly after removal podraznyka . Sounding pretty thin bottom cavity in case of acute deep caries sensitive because of the proximity Pulpi , while the average for acute caries more sensitive sensing is a wall cavity.

Chronic secondary caries in children sometimes have differentiated  yuvaty chronic form of periodontitis. The peculiarity of the current re- riodontytu children may be its development in a closed cavity of the tooth. This odiyiakovoyu measure applies to temporary and permanent teeth. When differentiating pay attention to the color of the tooth , and the reactiontion of the child during cavity preparation ( if performed without anesthesia ). In chronic periodontitis, especially permanent tooth , its color changes to gray. Prepaing enamel- dentinal connection is not accompanied by painfully  we sensations. These characteristics are the basis for radiographs of the affected tooth, which allows you to put the final diagnosis.

Radiography is used to diagnose and sometimes in hovanyh cavities located in aproksymalnyh in  upper teeth and invisible during the inspection .

Deep caries in permanent teeth of children diagnosed frequently. This stage is characterized by the decay that the pulp remains the halls thin layer of dentin. Pathologic changes detected in odontoblasts and pulp basic substance , congestion and round -vascular inflammatory infiltrates. Cavities located within prypulpovoho dentin. Therefore, probing her bottom quite sensitivelyve . Children may also complain of pain on thermal and mechanical stimuli are  , which passes quickly after their removal.

Differential diagnosis . Differentiate acute deep caries of permanent teeth should first of chronic fibrous pulpitis , pulp hyperemia and limited acute pulpitis , chronic form of periodontitis.

The main difference from caries pulpitis is the lack of wide  free twinge . Therefore, when collecting medical history should carefully examine whether there was a ever a pain. In addition, for Pulpitta characteristic pain of longer stimuli. Therefore, during the protermodiahnostyky maintenance should pay attention to the duration of paining sensation after removal of the stimulus. If the pain does not decrease immediately ¬ peared , and takes some time, it is a sign of pulpitis. After cavity preparation should carefully examine its bottom. The presence at the bottom of the cavity area pronounced softening of the dentin , and sharp pain in the sensing area that is featured ¬ ing chronic fibrous pulpitis. During the differential diagnosis invincibly ¬ whom caries and chronic fibrous pulpitis should be considered and each state physical health of the child. Certainly, children who HVO  riyut chronic diseases of internal organs, with sub- or – Dekom pensovanu form of caries activity , often justified by the diagnosis “chronic fibrous pulpitis ” with considerable depth of carious cavity nyny .

For the differential diagnosis of permanent teeth to the current root method can be applied elektrodontodi – agnostic. Indicators elektrozbudzhuvanosti pulp normally not ne ¬ exceeds 2.6 mA. In the case of pulpitis , this figure increased to ¬ schuyetsya 25-40 mA.

Acute caries

Acute caries is a rapid process involving a large number of teeth. These lesions are lighter colored than the other types, being light brown or grey, and their caseous  consistency makes the excavation difficult. Pulp exposures and sensitive teeth are often observed in patients with acute caries. It has been suggested that saliva does not easily penetrate the small opening to the carious lesion, so there are little opportunity for buffering or neutralization.

Chronic caries

These lesions are usually of long-standing involvement, affect a fewer number of teeth, and are smaller than acute caries. Pain is not a common feature because of protection afforded to the pulp by secondary dentin. The decalcified dentin is dark brown and leathery. Pulp prognosis is hopeful in that the deepest of lesions usually requires only prophylactic capping and protective bases. The lesions range in depth and include those that have just penetrated the enamel.

Arrested caries

Caries which becomes stationary or static and does not show any tendency for further progression. Both deciduous and permanent affected. With the shift in the oral conditions, even advanced lesions may become arrested. Arrested caries involving dentin shows a marked brown pigmentation and induration of the lesion.

Sclerosis of dentinal tubules and secondary dentin formation commonly occur  Exclusively seen in caries of occlusal surface with  large open cavity in which there is lack of food retention. Also on the proximal surfaces of tooth in cases in which the adjacent approximating tooth has been extracted.

3.     Based on virginity of lesion

·        initial/primary

·        recurrent/secondary

Primary caries(initial)

A primary caries is one in which the lesion constitutes the initial attack on the tooth surface. The designation of primary is based on the initial location of the lesion on the surface rather than the extent of damage.

Secondary caries (recurrent)

This type of caries is observed around the edges and under restorations. The common locations of secondary caries are the rough or overhanging margin and fracture place in all locations of the mouth. It may be result of poor adaptation of a restoration, which allows for  a marginal leakage, or it may be due to inadequate extension of the restoration. In addition caries may remain if there has not been complete excavation of the original lesion, which later may appear as a residual or recurrent caries.

4.     Based on extent of caries

·        incipient caries

·        occult caries

·        cavitation

Incipient caries

The early caries lesion, best seen on the smooth surface of teeth, is visible as a ‘white spot’. Histologically the lesion has an apparently intact surface layer overlying subsurface demineralization. Significantly may such lesion can undergo remineralization and thus the lesion per se is not an indication for restorative treatment. These white spot lesion may be confused initially with white developmental defects of enamel formation, which can be differentiated by their position away from the gingival margin, their shape (unrelated to plaque accumulation) and their symmetry (they usually affect the contralateral tooth). Also on wetting the caries lesion disappear while the developmental defect persist

It is believed that bite wing and OPG radiographs along with noninvasive adjuncts like fiber optic  transillumination (FOTI),laser luminescence, electrical resistance method (ERM) are used for diagnosis these occlusal lesions. These lesion are not associated with microorganisms different to those found in other carious lesion.  These carious lesion seem to increase with increasing age. Occult carious lesion are usually seen with low caries rate which is suggestive of increase fluid exposure. It is believed that increased fluid exposure encourages remineralization and slow down progress of the caries in the pit and fissure enamel while the cavitations continues in dentine, and the lesions become masked by a relatively intact enamel surface. These hidden lesions are called as fluoride bombs or fluoride syndrome. Recently it is seen that occult caries may have its origin as pre-eruptive defects which are detectable only with the use of radiographs. Once it reaches the dentinoenamel junction, the caries process has the potential to spread to the pulp along the dentinal tubules and also spread in lateral direction. Thus some amount of sensitivity may be associated with this type of lesion. This may be generally accompanied by cavitation

5.     Based on tissue involvement

·        Initial caries

·        Superficial caries

·        Moderate caries

·        Deep caries

·        Deep complicated caries

Dental caries can be divided into 4 or 5 stages

1.    Initial caries: Demineralization  without structural defect. This stage can be reversed by fluoridation  and enhanced mouth hygiene

2.    Superficial caries (Caries superficialis):Enamel caries, wedge-shaped structural defect. Caries has affected the enamel layer, but has not yet penetrated the dentin.

3.    Moderate caries (Caries media): Dentin caries. Extensive structural defect. Caries has penetrated up to the dentin and spreads two-dimensionally beneath the enamel defect where the dentin offers little resistance.

4.  Deep caries (Caries profunda): Deep structural defect. Caries has penetrated up to the dentin layers of the tooth close to the pulp.

5.  Deep complicated caries (Caries profunda complicata) :Caries has led to the opening of the pulp cavity (pulpa aperta or open pulp).

6.    Based on pathway of caries spread

·        forward caries

·        backward caries

“Forward-backward” classification is considered as  graphical representation of the pathway of dental caries.

ENAMEL

First component of enamel to be involved in carious process is the interprismatic substance. The disintegrating chemicals will proceed via the substance, causing the enamel prism to be undermined. The resultant caries involvement in enamel will have cone shape. In concave surface (pit and fissures) base towards DEJ. In convex surfaces (smooth surface) base away from DEJ.

DENTIN

First component to be involved in dentin is protoplasmic extension within the dentinal tubules. These protoplasmic extension have their maximum space at the DEJ, but as they approach the pulp chamber and root canal walls, the tubules become more densely arrange with fewer interconnections. So caries cone in dentin will have their base towards DEJ.

Decay starts in enamel then it involves the dentin. Wherever the caries cone in enamel is larger or at least the size as that of dentin, it is called forward decay (pit decay). However the carious process in dentin progresses much faster than in enamel, so the cone in dentin tends to spread laterally creating undermined enamel. In addition decay can attack enamel from its dentinal side. At this stage it becomes backward decay.

7.    Based oumber of tooth surface involved

·       Simple – caries involving only one tooth surface

·       Compound – caries involving two surfaces of tooth

·       Complex – caries that involves more than two surfaces of a tooth

8.    Based on chronology

·       early childhood caries

·       adolescent caries

·       adult caries

It has been stated that over a lifetime, caries incidence i.e. the number of new lesions occurring in a year, shows three peaks-at the ages 4-8,11-19 and 55-65 years.

Early childhood caries

Early childhood caries would include, two variants: Nursing caries and rampant caries. The difference primarily exist in involvement of the teeth (mandibular incisors) in the carious process in rampant caries as opposed to nursing caries.

Classification of early childhood caries

Type I (MILD )

·        Involves molars and incisors

·        Seen in 2-5 years

·        Causeàcariogenic semisolid food +lack of oral hygeine

Type II (MODERATE)

·        Unaffected mandibular incisors

·        Soon after first tooth erupts

·        Causeàinappropriate feeding +lack of oral hygiene

Type III (SEVERE)

·        All teeth including mandibular incisors

·        Causeàmultitude of factors

Nursing caries

·        Seen in infant and  toddler

·        Affects primary dentition

·        Mandibular incisors are

·        not involved

Etiology: improper bottle feeding, pacifier dipped in honey/other sweetner

Rampant caries

·        Seen in all ages, including adoloscennce

·        Affects primary and permanent dentition

·        Mandibular incisors are also affected

Etiology (multifactorial): frequent snacks, sticky refined CHO, decreased salivary flow, genetic background

Teenage caries         (adolescent caries)

This type of caries is a variant of rampant caries where the teeth generally considered immune to decay are involved. The caries is also described to be of a rapidly burrowing type, with a small enamel opening. The presence of  a large pulp chamber adds to the woes, causing early pulp involvement

Adult caries

With the recession of the gingiva and sometimes decreased salivary function due to atrophy, at the age of 55-60 years, the third peak of caries is observed. Root caries and cervical caries are more commonly found in this group. Sometime they are also associated with a partial denture clasp.

9.    Based on whether caries is completly removed or not during treatment

Residual caries

Residual caries is that which is not removed during a restorative procedure, either by accident, neglect or intention. Sometimes a small amount of acutely carious dentin close to the pulp is covered with a specific capping material to stimulate dentin deposition, isolating caries from pulp. The carious dentin can be removed at a later time.

10.                       Based on tooth surface to be restored

Most widespread clinical utilization

O  for occlusal surfaces

M  for mesial surfaces

D for distal surfaces

F  for facial surfaces

B  for buccal surfaces

L   for lingual surface

Various combinations are also possible, such as MOD –for mesio-occluso-distal surfaces.

11.                       Black’s classification

Class 1 lesions:

·       Lesions that begin in the structural defects of teeth such as pits, fissures and defective grooves. Locations include

·       Occlusal surface of molars and premolars.

·       occlusal two thirds of buccal and lingual surfaces of molars and premolars.

Class 2 lesions:

·       They are found on the proximal surfaces of the bicuspids and molars.

Class 3 lesions:

·       Lesions found on the proximal surfaces of anterior teeth that do not involve or necessitate the removal of the incisal angle.

Class 4 lesions:

·       Lesions found on the proximal surfaces of anterior teeth that involve the incisal angle.

Class 5 lesions:

·       Lesions that are found at the gingival third of the facial and lingual surfaces of anterior and posterior teeth.

Class 6 (Simon’s modification):

Lesions involving cuspal tips and incisal

 

12.World health organization (WHO) system

In this classification the shape and depth of the caries lesion scored  on a four point scale

D1. clinically detectable enamel lesions with intact (non cavitated) surfaces

D2. Clinically detectable cavities limited to enamel

D3. Clinically detectable cavities in dentin

D4. Lesions extending into the pulp

Parental influence and dental treatment

Parents are vital for positive reinforcement over any treatment objective. Programmes of treatment must be designed to reduce any chances of making parents or their children feel guilty. Design of treatment programmes should also allow goals to be achieved one by one, never overloading parent or child.

Dentist-patient relationship

Each patient is a unique individual and should be treated as such. Overall, it is fair to conclude that while the technical skill of a dentist is of concern, the most important factors for a patient are gentle friendly manner, explanation of treatment procedures and the ability to keep pain to a minimum. The structure of the dental consultation:

1. Greeting – by name

2. Preliminary chat: non-dental topics first, then dental; listen to the answers!

3. Preliminary explanation: clinical and preventive objectives in language that can be understood

4. Business: during treatment, constantly check the patient is not in pain and explain and discuss what you are doing; summarise what you have done to patient and parent and offer aftercare advice 5. Health education: constantly reinforce advice about maintaining a healthy mouth and give advice as though you mean it; always set realistic objectives

6. Dismissal: a clear signpost that the appointment is over, using the child’s name and a definite farewell.

 Anxious and unco-operative children

The extent of anxiety does not relate to dental knowledge but is an amalgam of personal experiences, family concerns, disease levels and general personality traits. It is, therefore, not easy to pinpoint aetiological agents and measure anxiety. In addition, there is no standard measure of anxiety. Helping anxious patients cope Several approaches can help to reduce coping problems: • reducing uncertainty — tell, show, do   send letter home explaining details of proposed visit  acclimatisation programmes modelling: videos or a live model  cognitive approaches  identification of beliefs: try to get individuals to identify and alter their dysfunctional beliefs, useful for all focused types of anxiety  distraction attempts to shift attention from dental setting towards another kind of situation, e.g. videos, headphones with music or stories  relaxation: useful for high levels of tension; aims to bring about deep muscular relaxation; trained therapist is required  systematic desensitisation: working through various levels of feared situations from ‘mildest’ to ‘most anxiety’ inhalation sedation: usually for ages 5 and over.

Care programme

History involves social, medical and dental information

Social. Name, address, age, school, siblings, parental occupations. This allows clinician to establish rapport. Try and assess social background, knowledge of dentistry and the family’s expectations.  Medical. Apart from allowing safe delivery of dental care, two additional factors can be gleaned: children with medical conditions may have a negative attitude to treatment because of the time they have spent in hospitals; they may also be more likely to fail dental appointments owing to the disruption in education that the medical problem has already caused.

Dental. Past dental experiences may give an indication of how the child will cope with proposed treatment. Parental attitude to treatment is important. A treatment plan must be modified to accommodate this. Establish exactly why they have come. The answers from child and parent may be different!

Examination

1. Clinical examination

The clinical examinatioeed not involve sitting in the dental chair at the first visit. Examine the child as a persoot just a mouth. Extraoral. General appearance is noted; percentile charts are useful way of monitoring height and weight. The head and neck is examined making a sketch of any lesions/marks. Intraoral. Soft tissues may be indicator of systemic disease. The relationship between periodontal condition and oral hygiene may indicate an underlying condition. Occlusion factors include crowding, malalignments, mandibular deviations and habits. The condition of the teeth is noted; are they clean and dry?

2. Radiographic examination

Guidelines for prescription of radiographs in children are shown in Table 13. There are 3 general indications for taking radiographs in children. Caries diagnosis. At least 50% more approximal lesions can be diagnosed by bitewing radiographs than with clinical examination. New orthopantogram (OPT) films may be very efficient at diagnosing occlusal caries, but bitewings remain essential in diagnosis of ‘occult’ occlusal caries. Abnormalities in dental development. All children at age 8 or 9 years should have an OPT to identify disturbances in development of the dentition in terms of the number, position and form of the teeth. Precise location of maxillary canines can then be achieved by intraoral parallex technique. Detection of bony or dental pathology. Periapicals examined for individual teeth; panoramic views for larger pathology or trauma.

3. Special investigations

There a number of special tests that are sometimes relevant:  vitality testing: not suitable for primary dentition; in permanent dentition, no tests are reliable but the electric pulp tester is probably the best  culture and sensitivity: bacterial, fungal and viral infections  blood tests: haematological, biochemical, bacteriological and virological examination.

Treatment planning

Planning should incorporate, management of pain, consider all teeth of poor prognosis  long-term treatment planning, to include attitudes and motivation preventive care, tailored to each individual  restorative care, realistic aims are important, aesthetic considerations, children can be under considerable peer pressure over their appearance.

 

 

 Prevention

The four practical ‘pillars of prevention’ are: diet, fluoride, fissure sealants and plaque control.

1. Dietary factors

Fluoride is the only dietary nutrient that has any preemptive influence on a tooth’s future susceptibility to caries (major effect is posteruptive). Non-milk extrinsic sugars (NME) are the dietary threat: sucrose, glucose, fructose, maltose. Intrinsic sugars (lactose in milk and sugars in fruit and vegetables) are not generally a threat to dental health. However, even lactose in milk in a bottle at night or in on-demand breast feeding can be cariogenic. Starchy staple foods (potatoes, bread, rice, pasta) are not a cause of dental caries, but mixtures of finely ground heat-treated starch and sugars (biscuits) are likely to be cariogenic. The frequency of sugar intake and the total quantity of sugar intake are important. In British schoolchildren two-thirds of NME intake is from confectionery, soft drinks and table sugar. Unnecessary addition of extra sugars to milk and other feeds is the cause of caries in young children, especially in immigrant minorities. Non-sugar sweeteners allowed for use in food and drinks can be considered for practical purposes as noncariogenic. A very slow metabolism for some bulk sweeteners in plaque is not important. There are two groups of non-sugar sweeteners

 • bulk: sorbitol, mannitol, isomalt, xylitol, lactitol and hydrogenated glucose syrup

• intense: saccharin, acesulphame K, aspartame, thaumatin. Bulk sweeteners have a laxative effect and should not be given to children under the age of 3 years.

Dietary advice

Dietary advice should be positive, practical and personal to the patient and parent, and take into account cooking skills and financial considerations. It can only be achieved with a written 3- or 4-day diary history. Advise against drinks with a high sugar content and titratable acidity. NMEs should be kept to main meals and acceptable alternatives should be suggested for between meal snacks. No food or drink should be taken within 1 hour of bed and no drink should be available (apart from water) during night.

2. Fluoride

Fluoride has the ability to increase enamel resistance to demineralisation as well as decreasing acid production in plaque and increasing remineralisation. Although it has a preeruptive effect its major role is posteruptive. Fluoride can be delivered systemically (swallowed) or topically (applied to the teeth). Water, salt and milk have and are being used throughout the world as systemic vehicles for fluoride. In the USA, 56% of the population receive fluoridated water, in Ireland 60% and in the UK 10%. Fluoride drops/tablets, which have a topical and a systemic effect, are an established and proven method of fluoridation. However, there has been a recommended daily reduction in dosage during the 1990s because it is recognised that the original dose was probably too high and that fluoride is now more likely to be ingested from other sources (toothpaste and water). Toothpastes have been responsible worldwide for the large fall in caries. In 1970, virtually no toothpaste contained fluoride; by 1978, 97% contained fluoride. Most adult pastes contain 1000–1500 ppm fluoride ions (used by those over age 5 years). Children’s pastes containing up to 500 ppm are available for those under 5. Only a smear of paste should be used and supervision of brushing is needed to prevent swallowing as this is a risk for fluorosis. Fluoride mouthrinses for age 6 years and over are a valuable daily adjunct. The 0.05% NaF ( ~ 225 ppm F–) mouthrinse probably has better compliance than weekly 0.2% NaF ( = 900 ppm NaF) application. Finally, professionally applied fluoride solutions, gels and varnishes complete the fluoride armamentarium. Varnishes are easier to apply than the solutions and gels and can be applied effectively to all ages. Although each individual method of fluoride application is effective, a combination of methods may achieve greater benefit (Table 14).

3. Fissure sealing

The most effective sealant is bis-GMA. At least 50% of sealants are retained for 5 years and their effectiveness in reducing and delaying the onset of caries is not in doubt. Both unfilled and filled resins and clear and opaque resins have been used to equal effect. Isolation after etching and drying is essential to success. Indications for patient selection and tooth selection

are: special needs: medical, physical, intellectual, social disability  caries in primary dentition  occlusal surfaces of permanent molars, cingulum pits of upper incisors

 

• seal as soon as moisture control permits  continue to monitor sealed teeth clinically and radiographically.

4. Plaque control

Caries reduction cannot be achieved by tooth brushing alone. However, toothbrushing will control gingivitis and periodontal disease and is an important way of conveying fluoride to the tooth surface. Chemical control of plaque with chlorhexidine is effective, but because of its side-effects (staining of teeth, altered taste sensation) it should only be used as a short term adjunct to periodontal care. The effects of all the practical ‘pillars of prevention’ are additive and all treatment plans should take into account age, caries risk, water fluoride level and cooperation.

Primary teeth

Pit and fissure caries

The primary fissures are shallower than their permanent counterparts and the presence of caries is a sign of high caries activity. The material of choice is an adhesive material either a GIC, resin-modified GIC, or compomer. Manufacturers’ instructions for these materials should be followed assiduously utilising tooth conditioners and bonding resins where stated.

 

 

 

 

Approximal caries

Minimal approximal cavity. A minimal approximal cavity with no occlusal dovetail is repaired using the retentive box preparation’. The material of choice is a compomer, which has greater mechanical strength than GIC or resin-modified GIC and which still releases fluoride. The approximal box is prepared as in Box 20 but without an occlusal dovetail. Additional retention grooves may be achieved by placing grooves into dentine using half-round burs along the gingival floor and lingual wall. The buccal wall is avoided because of the large buccal pulp horn in primary molars (Fig. 79).

Approximal caries with occlusal extension. The success rate of amalgam in approximal caries with occlusal extension has been reported as being 70-80%. (Box 20).

 

The failure rate of GICs is higher than amalgam: 33% over 5 years compared with 20% for amalgam. Consequently, amalgam is still the material of choice. However, recent clinical trials of 3 years’ duration show that compomers can be as durable as amalgam.

 

Restorations on more than two surfaces. Restorations extending onto more than two surfaces include cusp replacement and endodontically treated teeth. The stainless steel crown is the material of choice, with survival times in excess of 40 months. Their replacement rate is low at 3% compared with 15% for amalgams. Although initially they are more expensive, in the long term they are cost-effective. Problems of colour are gradually being overcome by the introduction of tooth-coloured veneer crowns. Once learnt, their placement technique (Box 21) is less technically demanding than intracoronal restorations in primary teeth and they should certainly be considered for any tooth for which the dentist cannot be sure that an alternative restoration would survive until the tooth is exfoliated.

Anterior teeth

Treatment options for anterior teeth depend on the severity of the decay and the age and co-operation of the patient. In the pre-school child, caries of the upper primary incisors is usually a result of ‘nursing caries syndrome’: frequent or prolonged consumption of fluids containing NME sugars from a bottle or feeder cup. Progression of decay is rapid, commencing on the labial

Fig. 80 Posterior caries with pit and fissure caries, (a) Position of the caries, (b) Removal of the occlusal caries, (c) Access to the approximal caries (sliver of enamel left), (d) Establish gingival floor of box and remove remaining enamel at the contact point, (e) Deepen the axio-pulpal line angle centrally as shown (f) in the cavity profile. The buccal and lingual walls of the cavity should be just clear of the broad contact areas. surface and quickly encircling the teeth. The most suitable form of restoration is the ‘strip crown technique’, which uses a celluloid crown former with light-cured composite resin to restore crown morphology. In older children over 3 or 4 years of age, new lesions of primary incisors indicate high caries activity. These lesions usually occur approximally and do not progress as quickly as nursing caries. They can be restored with GIC, compomer or composite resin.

 

Permanent teeth

Bitewing radiographs should be taken prior to any instrumentation of a tooth surface. For a clean fissure with no radiographic evidence of caries, a fissure sealant is the treatment of choice in molar teeth. If the fissure is stained with no radiographic evidence of caries, it will require clinical exploration. If clinical exploration reveals dentinal caries, then a restoration will be required. If dentinal caries is detected radiographically, a restoration is obviously necessary.

Fissure sealants

Consideratioeeds to be given whether to use a clear, coloured or opaque resin sealant or whether to use a non-filled or filled resin  Early sealants were clear in order to check that caries was not developing under the sealant. However, the margins were difficult to see and coloured and opaque materials were introduced in order to see areas of sealant fracture and loss. The final choice is with the individual clinician. Bitewing radiographs are an important part of sealant review as it only needs failure of one small part of the sealant-enamel bond for leakage to occur. GIC may be useful as temporary sealants in individuals with highly active caries until teeth have erupted sufficiently to allow conventional sealants Indeed they are similarly applicable for patients in whom isolation for placement of conventional sealants is impossible. They may require more frequent replacement because of their brittleness in thin section but they will provide occlusal protection and a reservoir of fluoride for release to surrounding enamel.

Stained fissure with no radiographic caries

The fissure should be explored with a small round bur. If the lesion stays within enamel, a fissure sealant is placed. If the lesion extends into dentine the treatment is as for pit and fissure caries.

Pit and fissure caries

If occlusal contacts are retained on enamel in a pit and fissure caries, a composite restoration is applicable, taking the opportunity to fissure seal non-carious fissures; this is known as a ‘preventive resin restoration’  The durability of preventive resin restorations is proven to be as good as occlusal amalgam restorations and is achieved with removal of significantly less enamel. If the occlusal contacts are not retained on enamel, then amalgam is the material of choice as it will not wear significantly, nor will it wear opposing teeth. Technique for placement of a preventive resin Restoration Figure 81 shows the placement of a preventive resin restoration.

1. Local anaesthesia and isolation.

2. Access questionable fissure with a small high-speed diamond bur.

3. Remove carious dentine and enough enamel to allow complete caries removal.

4. Remove caries from deeper dentine with a slowspeed round bur.

5. Place GIC liner over dentine, extending it up to amelodentinal junction, light-curing if necessary. 6. Gel/liquid etchant is placed on enamel margins for 20 seconds, followed by wash and dry. It is not necessary to etch the liner, sufficient roughening of the surface of GIC will result from washing. 7. Place a thin layer of bonding resin into the cavity and onto enamel margins. Cure for 20 seconds. 8. Incrementally fill the cavity with hybrid composite resin. Polymerise the resin until it is level with the occlusal surface.

9. Flow opaque unfilled fissure sealant over the restoration and the entire occlusal fissure pattern and cure for 20 seconds.

10. Check the occlusion.

Approximal caries

Amalgam remains the material of choice even in modern conservative cavity designs that do not sacrifice as much sound tissue as Black’s original designs. Nonmetallic restorative materials in these situations show significant wear after 4-5 years, which may be a manifestation of fatigue within the resin matrix.

Anterior teeth

Composite resin or the newer reinforced compomers should be the materials of choice. Incisal edge restorations require careful design to utilise more surface area of normal enamel rather than resorting to dentine pins.

 

The colour of a young persons teeth is of great importance. Peer group pressure can be significant, and teasing about size, position and colour of teeth can be very harmful. The most useful method of classification for the clinical management of discoloration is one that identifies the main site of discoloration  Once the aetiology has been identified, the most appropriate method of treatment can be chosen. Treatment emphasis should be on minimal tooth preparation. As a general rule, microabrasion should be the first-line treatment for all cases of enamel opacities and mottling; composite resin in the form of localised or full veneers is used in preference to porcelain.

Treatments

1.     Based on treatment and restoration design (black’s)

Class 1 restoration:

·       include the structural defects of teeth such as pits, fissures and defective grooves.

·       Locations include

·       Occlusal surface of molars and premolars.

·        occlusal two thirds of buccal and lingual surfaces of molars and premolars.

·       Lingual surfaces of anterior tooth.

Class 2 restoration :

They are found on the proximal surfaces of the bicuspids and molars.

Class 3 restoration :

·        restoration on the proximal surfaces of anterior teeth that do not involve or necessitate the removal of the incisal angle.

Class 4 restoration :

·        restoration on the proximal surfaces of anterior teeth that involve the incisal angle.

Class 5 restoration :

·        restoration at the gingival third of the facial and lingual surfaces of anterior and posterior teeth.

Class 6 (Simon’s modification):

·        restoration involving cuspal tips and incisal edges of teeth.

2.     Other modifications

Charbeneu’s modification:

a)    Class 2: cavity on single proximal surface of bicuspids and molars

b) Class 6: cavities on both mesial and distal proximal surfaces of posterior teeth that will share a common occlusal isthmus

c) Lingual surfaces of upper anterior teeth.

d) Any other unusually located pit or fissure involved with decay.

3. Sturdevant’s classific

·        Simple cavity – cavity involving only one tooth surface

·        Compound cavity- cavity involving two surfaces of tooth

·        Complex cavity – cavity that involves more than two surfaces of a tooth

4 .Finn’s modification of Black’s cavity preparation for primary teeth

·        Class1 : Cavities involving the pits and    fissures of molar teeth and the buccal and lingual pits of all teeth.

·        Class 2: cavities involving proximal surface of molar teeth will access established from the occlusal surface.

·        Class 3: cavities involving proximal surfaces of anterior teeth which may or may not involve a labial or a lingual extension

·        Class 4: a restoration of the proximal surface of an anterior tooth which involves the restoration of an        incisal angle.

·        Class 5: cavities present on the cervical   third of all teeth, including proximal surface where the         marginal ridge is not included in the    cavity preparation.

The four sizes of carious lesions

·       Size1:Minimal involvement of dentin just beyond treatment by remineralization alone.

§     Size 2: Moderate involvement of dentin. Following cavity   preparation, remaining enamel is sound, well supported by dentin and not likely to fail under normal            occlusal load. The remaining tooth     structure is sufficiently strong to support the restoration.

§     Size 3: the cavity is enlarged beyond moderate. The remaining tooth structure is          weakened to the extent that cups or incisal edges are split, or are likely to fail or left exposed to occlusal or incisal load. the cavity needs to be further enlarged so that the restoration can be designed to provide support and protection to the remaining tooth structure.

§     Size4: Extensive caries with bulk loss of tooth structure has already occurred.

 

 

 

 

 

Treatments for discoloured teeth can be used in children and adults, although some are not suitable for children younger than teenage. Techniques use abrasion, bleaching and restorations. The exact mechanism by which bleaching occurs remains unknown. Theories of oxidation, photo-oxidation and ion exchange have been suggested.

The hydrochloric acid pumice microabrasion technique

The microabrasion method is a controlled removal of surface enamel in order to improve discolorations that are limited to the outer enamel layer  It is achieved by a combination of abrasion and erosion and the term ‘abrosion’ is sometimes used. No more than 100 μm of enamel are removed. Once completed, the procedure should not be repeated. Too much enamel removal is potentially damaging to the pulp and cosmetically the underlying dentine colour will become more evident.

Indications

• fluorosis

• idiopathic speckling

• postorthodontic demineralisation

• prior to veneer placement for well-demarcated stains

• white/brown surface staining, e.g. secondary to

primary predecessor infection or trauma (Turner teeth).

Effectiveness

Critical analysis of the effectiveness of the technique should not be made immediately but delayed for at least

1 month as the appearance of the teeth will continue to improve over this time. Experience has shown that although white mottling is often incompletely removed it does become less perceptible. This phenomenon has been attributed to the relatively prismless layer of compacted surface enamel produced by the ‘abrasion’ technique, which alters the optical properties of the tooth surface. Long-term studies of the technique have found no association with pulpal damage, increased caries susceptibility or significant prolonged thermal sensitivity. Patient compliance and satisfaction is good and any dissatisfaction is usually a result of inadequate preoperative explanation. The technique is easy to perform for operator and patient and is not time consuming. Removal of any mottled area is permanent and is achieved with an insignificant loss of surface enamel. Failure to improve the appearance by the microabrasion technique does not have any harmful effects and may make it easier to mask some lesions with veneers.

 ETIOLOGY

Historical studies

In 1883 Miller showed that carbohydrates when incubated with saliva caused demineralisation of extracted teeth. This showed for the first time that there was some scientific basis for dental caries being caused by diet. In 1940 studies by Stephan showed that dental plaque had a resting pH of 6.5–7; when exposed to fermentable sugars, such as sucrose, glucose or fructose, the pH fell rapidly to a pH well below 5, followed by a slow recovery to the original level over the next 30–60 minutes.

Teeth tissues are the most vulnerable during final mineralization. In this case the most important role plays nutrition, lack amount of vitamin D and minerals, including calcium and fluoride in the body, hormonal and metabolic system diseases as general factors. An origin and development of the caries process is influenced also by such factors: presence of orthodontic pathology, high viscosity of saliva, insufficient buffering properties of saliva.

MICROBIOLOGY

Substantial evidence indicates that streptococci are essential for development of caries, particularly of smooth (interstitial) surfaces. These are viridans streptococci which are a heterogeneous group including Streptococcus mutans, S. sobrinus, S.salivarius, S. mitior and S. sanguis.

Viridans streptococci vary in their ability to attach to different types of tissues, their ability to ferment sugars (particularly sucrose), and the concentrations of acid thus produced. They also differ in the types of polysaccharides that they form. Certain strains of S. mutans are strongly acidogenic and, at low pH, with freely available sucrose, also store an intracellular, glycogen-like, reserve polysaccharide. When the supply of substrate dries up, this reserve is metabolised to continue acid production for a time. Drastic reduction in dietary sucrose intake is followed by virtual elimination of S. mutans from plaque and reduces or abolishes caries activity. When sucrose is made freely available again S. mutans rapidly recolonises the plaque.  However, simple clinical observation of the sites (interstitially and in pits and fissures) where dental caries is active, shows that the bacteria responsible are not those floating free in the saliva. Dental caries develops only at the interface between tooth surface and dental plaque in stagnation areas.

Saliva  affects  caries  etiology  through  the  rate  of  secretion  and  composition.  Saliva affects  the  integrity  of  teeth  by the  composition  of  (buffer  system,  calcium  and phosphate). By the cleansing action of saliva (oral clearance), it can affect the number of oral microorganisms and food debris from  the mouth. The oral immune system (specific and non specific) affect to a large degree the cariogenic bacteria.

It is the acidic pH that demineralises enamel and dentine. The critical pH for enamel is around 5.2–5.5 while for dentine it is around pH 6.0. The critical pH is defined as the pH at which the tooth tissue loses mineral to the saliva or plaque. The differences in pH are important in determining the rate of progression of enamel and root caries.

PATHOGENESIS

Clinically, bacterial plaque is a tenaciously adherent deposit on the teeth. It resists the friction of food during mastication, and can only be readily removed by toothbrushing. However, neither toothbrushing nor fibrous foods will remove plaque from inaccessible surfaces or pits (stagnation areas). Plaque becomes visible, particularly on the labial surfaces of the incisors, whentoothbrushing is stopped for 12-24 hours. It appears as a translucent film with a matt surface that dulls the otherwise smooth and shiny enamel. It can be made obvious when stained with disclosing agents. In stagnation areas where it is undisturbed, plaque bacteria can form acid from sugars over sufficiently long periods as to attack tooth surfaces. Adhesion of bacteria to the teeth from which they would otherwise be washed away is an essential requirement for the colonisation of enamel.

THE EPIDEMIOLOGY OF CARIES

It cannot be stated too often that dental caries has a multi-factorial aetiology and the factors that have been identified as important in the development of caries are the consumption of fermentable sugars, the microflora of the dental plaque and the tooth surface.The prevalence and incidence of dental caries in a given population and in an individual are dependent upon the outcome of the interactions of these factors. These individual factors are, in turn, determined by a number of apparently unrelated factors which necessarily impact on them. The frequency of use of fluoride-containing toothpastes, which modify the tooth surface and may influence the acidogenicity of dental plaque, and the frequency of consumption of fermentable sugars by children may both, for example, be determined by the educational level and income of apparent, while the availability of fluoride-containing tooth-pastes may be determined by the commercial policy of the toothpaste producer.

INDICES OF DENTAL CARIES

Research over the years has shown that caries is a preventable and controllable disease. To apply measures which can prevent or control caries, a reliable picture of it in a population is prerequisite; this can only be obtained if we have a reliable caries assessment system (index).

For  several  decades  dental  researchers  are following  and  teaching  DMF  index  developed  by Klein, Palmer and Knutson in 1938 for assessing dental  caries.  World  health  organization  has adopted  this  index  in  its  oral  health  assessment form  for conducting  national  oral  health  surveys [16]. Various reasons can be stated for its continued use for assessing caries, foremost of them are: it is simple to use, valid and reliable, that is why it is still being used for assessment and comparison of caries status of the population groups around the world.

MEASUREMENT OF INTENSITY OF CARIES

*Permanent teeth index:

The DMF index is the average number of permanent teeth per person which are decayed (D), missing because of caries (M), or filled (F). It is a quantitative expression of the life-time caries experience of the permanent teeth. In the calculation of the DMF index, the numerator is the total number of DMF teeth and the denominator is the total number of persons examined.

Decayed-Missing-Filled  Index  (  DMF  )  which  was  introduced  by  Klein, Palmer and Knutson in 1938 and modified by WHO:

 

1-DMF  teeth  index  (DMFT)  which  measures  the  prevalence  of  dental caries/Teeth.

2- DMF surfaces index (DMFS) which measures the severity of dental caries.

 

The components are:

D  component: 

Used to describe (Decayed teeth) which include:

1.  Carious tooth.

2.  Filled tooth with recurrent decay.

3.  Only the root are left.

4.  Defect filling with caries.

5.  Temporary filling.

6.  Filled tooth surface with other surface decayed.

 

M   component: 

Used to describe (Missing teeth due to caries) other cases should be excluded these are:                               

1.  Tooth  that  extracted  for  reasons  other  than  caries  should  be  excluded,

which include:      

a-Orthodontic treatment.

b-Impaction.

c-Periodontal disease.

2.  Un-erupted teeth.

3.  Congenitally missing.

4.  Avulsion teeth due to trauma or accident.

 

F   component:

Used  to  describe  (Filled  teeth  due  to  caries).  Teeth  were  considered  filled without decay when one or more permanent restorations were present and there was  no  secondary  (recurrent)  caries  or  other  area  of  the  tooth  with  primary caries. A tooth with a crown placed because of previous decay was recorded in this  category.  Teeth  stored  for  reason  other  than dental  caries  should  be excluded, which include:

1.  Trauma (fracture).

2.  Hypoplasia (cosmetic purposes).

3.  Bridge abutment (retention).

4.  Seal a root canal due to trauma.

5.  Fissure sealant.

6.  Preventive filling.

DIAGNOSTIC METHODS FOR DENTAL CARIES

Clinical methods

Caries occurs on the occlusal, aproximal and buccal/lingual surfaces of teeth. On smooth surfaces the lesions normally develop close to the gingival margin and are often covered in plaque. Those developing in fissures and aproximal surfaces are more difficult to detect and diagnosis usually involves indirect methods. Diagnostic tests have been developed to maximise the accuracy of caries detection on each surface. On the buccal and lingual surfaces the optimal assessment is the visual appearance of the surface. A white spot lesion can be seen when enamel has been cleaned and dried. The area is often  covered in plaque. On those surfaces hidden from direct visual examination, radiographic examination is the most commonly used diagnostic technique.

Radiography

Bitewing radiographs are relatively reliable for detecting aproximal lesions but less so for occlusal lesions. Radiolucenciesdeveloping below the contact areas appear like horizontal V-shaped notches in enamel-only lesions. As the lesion progresses into dentine,  a mushroom formation occurs as the enamel appears to be undermined along the enamel–dentine junction (EDJ). The situation is more difficult to assess on the occlusal surfaces as the more mineralised and thicker enamel partly obscures the lesion progression. The advancing lesion is therefore relatively underdiagnosed by radiographs. A rough guide suggests that a lesion is 25% more advanced than when estimated from a radiograph. A bitewing radiograph needs to be taken correctly to have the most diagnostic yield. Film holders yield the most accurate results and ensure that the X-rays pass perpendicularly through the crown of the tooth. This reduces the amount of overlap. A clear outline should be visible of the enamel overlying the dentine and allows good distinction between the two tissues. A clear change in the radiolucency of the tooth can then be seen. Caries appears as radiolucent shadowing and occurs at susceptible sites. Aproximally, this will occur below the contact area and above the alveolar bone. Beneath the occlusal surfaces the faint outline of caries can be detected. The radiolucent zone appears as a diffuse zone beneath the enamel. The extent of the lesion spread is more difficult to visualise as the bulk of the enamel and dentine partly obscures the X-rays; this results in a less accurate assessment of occlusal caries compared to that occurring aproximally. The frequency of bitewing radiographs should be assessed for each individual. A high caries risk individual might require radiographs taken at yearly intervals whereas someone with no caries experience for a number of years would need them less frequently, e.g. every 4–5 years.

Transillumination

This is a rarely used technique to assess caries on molars and premolars but more commonly used on anterior teeth. Direct light reflected by dental mirrors on to the teeth can highlight darkened shadows present between the aproximal surfaces of upper anterior teeth. A carious lesion shows as a darkened shadowed area in dentine surrounded by a normal coloured zone. Light curing lamps can be used to examine the surfaces as white  intraoral lights are not common. These lights need to be directed between the contacts of teeth and have sufficient intensity to show the caries. Generally, ambient light sources need to be reduced to improve the reliability of the diagnosis.

New techniques

Electronic caries meters

Recent research has suggested that changes to the electrical impedance of enamel can indicate an active lesion. Small d.c. voltages have less resistance in carious enamel than that through an intact surface. The instrument needs a clean and dry surface to work efficiently and is generally used on the occlusal surfaces of molars and premolars. The advantage of using this technique is that it is the occlusal surfaces of molar and premolar teeth where radiographic assessment of caries is less accurate than the proximal surface. The tip of the probe is less than 1 mm in diameter and can detect changes in the impedance of enamel over very small areas. This means that over small areas the instrument might be very accurate at detecting early carious lesions, but the reliability over larger areas has been questioned. If anything, this technique has the potential to overdiagnose caries by giving false-positive results and so has not resulted in widespread usage.

DIAGNOdent

This technique, currently commercially available as an instrument called the DIAGNOdent (KaVo), utilizes the reflectivity of light from the tooth surface. The light reflectivity from a carious and non-carious surface is  different. The instrument is calibrated to detect this difference and informs the operator through a read out (Fig. 4.11). Like the electronic caries meters, these instruments can overdiagnose caries and potentially confuse stained surfaces with carious ones. In addition, some restorative materials have shown similar fluorescent values to those of carious dentine and its application for the detection of secondary caries seems questionable. As a result, these instruments have also not seen wide usage.

 

 

 

Treatment

The treatment of carious teeth should be based on the needs of the child; the long-term objective should be to help the child to reach adulthood with an intact permanent dentition, no active caries, as few teeth restored as possible and a positive attitude toward their future dental health.

Restorative materials:

Amalgam. Its main advantage is that it is economical and simple to use. However, there is current concern over its safety. In Scandinavia, its use is banned in children, with concern over environmental issues rather than amalgam toxicity itself. It does seem prudent to avoid its use whenever possible, especially in the paediatric population where other materials may give sufficient longevity.

Glass ionomer cements (GIC). These consist of basic glass and acidic water-soluble powder; they set by an acid-base reaction between the two components. The cement bonds to enamel and dentine and releases fluoride to the surrounding tissues.

Resin-modified GIC. A hybrid of GIC/resin that retains significant acid-base reaction in its overall curing process to set in the dark. There are two setting reactions: the acid-base reaction between glass and polyacid and a light-activated, free radical polymerisation of methacrylate groups of the polymer. This material has some physical advantages over conventional GIC, together with its ability to ‘command set’.

Polyacid-modified composite resin (compomer). This contains either or both essential components of a resinmodified GIC but it is not water based and, therefore, no acid-base reaction can occur. They will not set in the dark and cannot strictly be described as GICs.

 Composite resins. Their introduction revolutionised clinical dentistry and their aesthetic benefits are unquestioned. Problems of resistance to wear, water absorption and polymerisation contraction have restricted their use in the permanent posterior teeth and almost ruled them out of a role in caries management in posterior primary teeth. Nevertheless they do have clearly defined roles in the anterior teeth of both dentitions.

Preformed crowns. These preformed extracoronal restorations are essential in the restoration of grossly broken down teeth, primary molars that have undergone pulp therapy, hypoplastic primary and permanent teeth and teeth in those children at high risk of caries, particularly those having treatment under general anaesthesia.

Isolation

Adequate isolation is necessary for any restorative material to have a chance of success. Rubber dam isolation is the optimum and may necessitate local anaesthesia for the gingival tissues. Clamps should be secured individually with floss ligatures. Additional advantages of the rubber dam include airway protection, soft tissue protection and reduced risk of caries infection from saliva aerosol. In the absence of rubber dam, good moisture control can be achieved with cotton wool rolls, dry tips and saliva ejector.

Mechanical measures

•         This refers to procedures specifically designed for and aimed at removal of plaque from tooth surface methods for cleaning tooth mechanically are:

1.     Prophylaxis by dentist

2.     Tooth brushing

3.     Mouth rinsing

4.     Use of dental floss or tooth picks

5.     Incorporation of detergents foods in diet

6.     Pit and fissure sealants

Dental prophylaxis

•         Careful polishing of roughened smooth surface and correction of faulty restoration decreases the formation of bacterial plaque and there by reducing the development of new carious lesion

Tooth brushing

Types of tooth brushing

–         Manual

–         Powered

–         Sonic and ultrasonic

–         Ionic

ADA specification for a tooth brush

–         1- 1.25 inches length

–         5/16 – 3/8 inches in width

–         2 – 4 rows of bristles

–         5-12 tufts per row

Mouth rinsing

•         Use of mouth wash for the benefit of its action in loosening food debris from teeth has been suggested to be of value as caries control measures.

Dental floss

•         Dental flossing is effective in removing plaque and dislodge the irritating matter that is real source of disease.

•         Used in type I gingival embrasures

It is available in:

–         Multifilament – twisted / non twisted

–         Bounded / unbounded

–         Thick / thin

–         Waxed / non waxed

Oral irrigators

–         Use of flushing devices

–         Irrigation devices composed of a built in pump and a reservoir

–         It can also be used to deliver antimicrobial agents

Detergent foods

•         Fibrous food in diet prevent lodging of food in pit and fissure and acts as detergent

Chewing gum

•         Chewing gum tend to prevent caries by mechanical cleaning action

Pit and fissure sealants

•         A sealant is a dental resin that is firmly bounded to enamel surface and isolates pit and fissure from caries producing conditions in oral environment

•         Types:
1^st generation – ultraviolet light activated

2^nd generation – chemical activated

3^rd generation – visible light activated

4^th generation – fluoride containing

•         Examples of pit and fissure sealants

•         alphadent

•         helioseal F

•         helioseal

•         Seal – rite

•         baritone L3

•         concise white sealant

•         concise light cure white seal