6. Dental

6. Dental caries. Classification of dental caries. Modern concept of the etiology and pathogenesis of dental caries. Anesthesia in the treatment of caries, methods, instruments, indications for use. Acute and chronic caries in the stage of spot (initial). Pathomorphology, clinic, diagnosis, differential diagnosis and treatment.

Dental Caries – is a complex pathological process that occurs after tooth eruption, with subsequent demineralization and softening of dental hard tissues, thus leading to further cavitation in a consequence of local and general factors.

Dental caries is the major cause for loss of teeth in children and adults. It affects the enamel surfaces of teeth in children and adults and the exposed root surfaces of the teeth of the elderly. Dental caries is the result of the interaction of the bacteria on the tooth surface, the dental plaque or oral biofilm, the diet and specifically fermentable carbohydrate components of the diet, which are fermented by the plaque microflora to organic acids (primarily lactic and acetic acids), and the teeth acting together over time. Dental caries will occur only when the three factors are present together and when they act together over a sufficient period of time.

Dental caries is a sugar-dependent infectious disease. Acid is produced as a by-product of the metabolism of dietary carbohydrate by plaque bacteria, which results in a fall in pH at the tooth surface. In response, calcium and phosphate ions diffuse out of enamel, resulting in demineralization. This process is reversed when the pH rises again.  Caries is – a dynamic process characterized by episodic demineralization and remineralization occurring over time. If destruction predominates, disintegration of the mineral component will occur, leading to cavitation.

Enamel caries The initial lesion is visible as a white spot. This appearance is due to demineralization of the prisms in a subsurface layer, with the surface enamel remaining more mineralized. With continued acid attack the surface changes from being smooth to rough, and may become stained. As the lesion progresses, pitting and eventually cavitation occur. The carious process favors repair, as remineralized enamel concentrates fluoride and has larger crystals, with a ↓ surface area. Fissure caries often starts as two white spot lesions on opposing walls, which coalesce.

Dentin caries comprises demineralization followed by bacterial invasion, but differs from enamel caries in the production of secondary dentine and the proximity of the pulp. Once bacteria reach the dentinoenamel junction (DEJ), lateral spread occurs, undermining the overlying enamel.

 

Fig. 1 Schematic diagram to demonstrate the requirement for diet, bacteria and dentition to interact together over time to

initiate caries.

 

CLASSIFICATION OF DENTAL CARIES:

1. Clinical: •   -initial (white spot lesion) •   -superficial (c. superficialis) •   -medium (c. media) •   -deep (c. profunda)

2. The anatomical: •   -caries of enamel •   -caries of dentine •   -caries of cement

3. On localization: •  -fissure •  -proximal •  -in the cervical part (circulating)

4. On a severity: • -acute • -chronic • -plural (rampant) • -secondary • -arrested (stopped)

5. On an intensity of lesion: •   -a compensated •   -a sub-compensated •   -a decompensated

6. On the presence of complications: • -simple • -complicated

Rampant  caries  on  the  other  hand  is  a  sudden  rapid  destruction  of  many  teeth, affecting surfaces that considered relatively immune to caries attack

Recurrent or secondary caries: Seen in the margins of an old restored area.

Arrested caries: Re mineralized carious lesion.

CLASSIFICATION OF CARIOUS CAVITIES

 

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, when toothbrushing 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.

 

Note :

1-  A  tooth  is  considered  to  be  erupted  when  just  the  cusp  tip  of  the  occlusal surface or incisor edge is exposed . The excluded teeth in the DMF index are:

a- Supernumerary teeth. 

b- The third molar according to Klein, Palmer and Knutson only.

 

2-Limitations – DMF index can be invalid in older adults or in children because

index can overestimate caries record by cases other than dental caries.

 

Principle and rules in recoding:

1-DMFT:

►-  A tooth may have several restorations but it counted as one tooth, F. 

►-  A tooth may have restoration on one surface and caries on the other, it should be counted as decayed   D .

►-  No tooth must be counted more than once, D M  F   or sound. 

 

2-DMFS

     Each  tooth  was  recorded  scored  as  4    surfaces  for  anterior  teeth  and  5 surfaces  for  posterior  teeth. 

  Retained  root  was  recorded  as 4  D  for  anterior teeth,  5  D  for  posterior teeth.

  Missing tooth was recorded as 4 M for anterior teeth, 5 M for posterior teeth.

  Tooth with crown was recorded as 4 F for anterior teeth, 5 F for posterior teeth.

 

Calculation  of  DMFT 

1- For individual                                                2- For population        

DMF = D + M + F                             

 

Maximum  score:                                                   Minimum  score = Zero  

1-  DMFT = 32                                                     

2-  DMFS =  12 * 4 + 20 * 5 

   = 48 + 100   =  148  or   128

 

 

Table. Level of dental caries intensity (DMFT index)

                                                       

*Primary teeth index:

 

1- dmft / dmfs                    

  Maximum scores:   dmft =  20    ,          dmfs = 88 

 

2- deft / defs , which was introduced by Gruebbel  in  1944

                                     d- decayed tooth .

                                     e- decayed tooth indicated for extraction . 

                                     f- filled tooth.

 

3- dft / dfs   

    In which the missing teeth are ignored, because in children it is difficult to

make sure whether the missing tooth was exfoliated or extracted due to caries or

due to serial extraction.                              

 

 Mixed dentition:

         Each child is given a separate index, one for permanent teeth and another for primary teeth.

Information from the dental caries indices can be derived to show the:

1.  Number of  persons affected by dental caries (%).

2.  Number of surfaces and teeth with  past and present dental caries (DMFT / dmft — DMFS / dmfs).                           

3.  Number  of  teeth  that  need  treatment,  missing  due  to  caries,  and have been treated ( DT/dt , MT/mt , FT/f t).

 

Q- How could you differentiate between tooth missing due to caries and due to exfoliation?

1-  By age of the patient if it is near to exfoliation time or not.

2-  The  shape  of  ridge  is  concave  in  carious  missing  tooth  and  straight  in

exfoliated one and permanent successor may be seen. 

3-  DMF/dmf index is higher in association with carious missing tooth 

especially adjacent and the contra lateral teeth.

     4- Bad oral hygiene mainly associated with carious teeth.

 

Q- How could you differentiate between tooth missing due to caries and due to orthodontic treatment?

 

1-  By type of teeth, in ortho. treatment most teeth should be extracted are 4,5/c, d while in carious missing teeth any teeth may be involved.

2-  Bilateral  and  /or  opposing  missing  generally  associated  with  ortho. treatment, while in carious missing teeth it is not necessary.

3-  DMF/dmf  index  is  higher  in  association  with  carious  missing  tooth especially  adjacent  and  the  contra  lateral  teeth  with  bad  oral  hygiene mainly associated with carious teeth.

4-  Crowding or appliance may be seen in ortho. treatment.

MEASUREMENT OF PREVALENCE OF CARIES

The first purpose is to provide a measure of the prevalence of clinical caries, of teeth missing due to caries or of filled teeth in terms of the proportion of persons affected. The calculation of this index involves a count of the number of persons with one or more cavities (clinical caries), with one or more teeth missing because of caries, or with one or more teeth filled. These numbers are divided by the number of persons examined and multiplied by 100 %. Such rates should be specifically for age and optionally for sex and ethnic groups. They should also be calculated separately for primary and permanent teeth. Prevalence rates of this type will provide answers to the following questions: What proportion of the people require treatment for clinical caries? What proportion of the people have teeth missing because of caries? What proportion of the people have teeth filled? What proportion of the people are caries-free?

MEASUREMENT OF INCIDENCE OF CARIES

The incidence of clinical caries in permanent teeth can be determined by conducting two surveys separated by a specified interval of time (usually one year). The difference between the meaumbers of DMF teeth at the first and second examinations is the incidence of dental caries for the specified period of time. This figure can be adjusted arithmetically so that the incidence can be expressed as the meaumber of newly decayed permanent teeth per person per year.

When age specific DMF rates are used it is possible to estimate the incidence of clinical caries in permanent teeth between any two ages, for example from 6 to 7 years, by subtracting the meaumber of DMF teeth per person at the younger age (6) from the meaumber of DMF teeth per person at the higher age (7).

 

Adult and childhood caries

In adults caries usually progresses slowly and small cavity may take several months to develop. By contrast, childhood caries, particularly of deciduous teeth, may be so rapid that the pulp becomes exposed long before the tooth is due to be shed.

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. Radiolucencies developing 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.

 

THE EARLY VISIBLE LESION.

 INITIAL DENTAL CARIES

WHITE SPOT LESION

The earliest visible changes are seen as a white opaque spot that forms just adjacent to a contact point. Despite the chalky appearance the enamel is hard and smooth to the probe.

Complaints: any complaints on the pain are absent; aesthetic defect only, especially if the lesion is on the cervical part of front group of teeth.

Objectively: white chalk-like spots, dull (lusterless) if it is acute process, brown – pigmented spots in the chronic course of the disease. Spots are localized as usual in fissures, pits, proximal surfaces and in the cervical part of teeth. During probing the surface of the spot is hard and smooth. Spot is stained with methylene blue solution – 2%.

Local Treatment: remineralisation therapy – affected surfaces are covered with solutions that contain fluoride.

Method: to clean the tooth with polishing brush and prophylaxis paste; dry the tooth surface with air; apply fluoride-containing solution to the tooth surface; patient is given a recommendatioot to eat for one hour, not to brush teeth this day. Second appointment in 2-3 days; procedure is repeated 3 times.

General treatment: medications that contain Calcium and Phosphorous in tablets. Diet with low consumption of carbohydrates; tooth-paste with fluoride, to remineralize enamel.

Clinical picture: white spot lesions.

 

 

Table 1.                                                             DIFFERENTIAL DIAGNOSIS OF INITIAL CARIES

 

Non-surgical management of dental caries

Prevention

The most important preventive roles are improving plaque removal and reduction in frequency of sugar  consumption. Oral hygiene instructions should aim to improve plaque removal and produce a reduction in the bacterial load in the mouth. Careful flossing techniques, although difficult to learn, are efficient at removing the cariogenic bacteria even from interdental areas. Although much of the emphasis in the UK is aimed at dietary reduction  of refined carbohydrates, other parts of Europe consider efficient tooth cleaning as important if not more so than dietary advice. Whichever is more important, efficient plaque removal reduces the bacterial load but, without changes to the diet by reducing the frequency of sugar intake, neither will be effective on their own. Dietary changes are notably difficult to achieve, but smaller less intrusive changes can be effective. Educational messages, such as reducing the frequency of sugar intake, particularly in drinks such as tea and coffee, can have significant impact. The concept of hidden sugars is also very important. These are sugars not necessarily immediately associated with caries. These sugars can be found in biscuits, crisps and other snack foods. Removing them from the diet can aid caries reduction.

Fissure sealants

Fissure sealants are a preventive technique for the management of pit and fissure lesions. They work by closing over the fissures and thus preventing the accumulation of plaque in pits and fissures, areas of the teeth which are difficult to keep plaque free. However, continuation of a cariogenic diet results in caries developing in adjacent sites next to the fissure-sealed areas. The unfilled or partially filled resin-based materials are not resistant to occlusal wear and will be gradually worn away over time and so may need replacing. However, the materials should be sufficiently flowable to pass into the occlusal fissures. Even though the occlusal surfaces may be worn away over time, residual parts within the deep occlusal fissures remain to protect the tooth. Fissure sealants are generally not indicated for all young patients and are usually targeted at those with a higher risk.

Indications for fissure sealants include:

■ High caries-risk patients.

■ Deep fissures.

■ Special needs patients.

Fissures may be sealed with either glass ionomers or resin composites but the failure rates for glass- ionomers are much higher.

FISSURE PRESSURIZING

This method is used to pressurize fissures in molars and premolars and natural pits, in teeth of children. It has generally been considered that pit and fissure surfaces of molar teeth usually become carious within 3 years of eruption because enamel is not mineralized yet in fissures (for kids of 6 -8 years old, whose fissures in molars are not enough mineralized). Sealants protect the occlusal surfaces of molar teeth, providing a smooth surface as the morphology of this surface makes it more susceptible to dental caries and  favouring plaque stagnation.

Types of materials:

►Acid-etch resin composite sealants (the same stages of applying as light-curing composites – etching, washing, drying stage and sealant placement with subsequent light-curing)

►Glass ionomer cements ( is used when it is difficult to achieve adequate moisture control, as this material is less sensitive to the presence of moisture; is easy to use on children, bonds well to enamel and releases fluoride, providing  a potentially cariostatic effect)

Methods:

Non-invasive (for not affected fissures in molars and premolars in teeth that are  2-3 years after eruption; age of children 6-8);

Non-invasive method of fissure pressurizing envisages applying of sealants to the fissures of tooth, that is only cleaned with brush and prophylaxis paste (without fissure preparation by burs) after tooth cleaning follows stage of sealant placement.  (see stages of pressurizing)

Invasive (for deep, pigmented fissures, but not affected by caries process)

Invasive method of fissure pressurizing

The same stages are held as in the non-invasive method, but after the tooth preparation, the stage of fissure disclosure is performed with small diamond bur for high-speed handpiece. After the fissure was disclosed,  it should be available for good visual examination and for next fissure pressurizing. Invasive method of fissure pressurizing differs from conventional carious cavity preparation by sparing teeth tissues preparation, especially enamel.

Stages of pressurizing:

Tooth preparation

The tooth to be fissure sealed must be plaque free and free from debris. This can be achieved using a prophylaxis cup or brush, with or without pumice or any non-fluoride, non-oil based paste, or by the use of air abrasion. Afterwards, the probe should be run through the fissure system to free any retained pumice. Following this, the tooth should be thoroughly washed and dried with a three-in-one syringe, and re-examined.

Tooth isolation

Good isolation to keep the teeth dry is critical to successful sealant restoration. A rubber dam to isolate the teeth will provide ideal isolation and will control movements of the tongue but is not always well tolerated by children.

An alternative is to use cotton wool rolls and dry guards; dry guards can be placed over the parotid ducts. Saliva ejectors and high-speed suction are also useful when used in conjunction with other isolation materials.

Moisture-free surface

The tooth needs to be completely dry prior to placement of the acid etchant. The presence of saliva or water compromises sealant bonding and subsequent retention.

Ensure that the three-in-one syringe tip is not contaminated with water coming out of the air tip when drying the tooth by testing on a dry tissue. The inability to obtain good isolation is a contraindication to providing fissure sealants.

Enamel etch

Phosphoric acid etchant gel is applied for the manufacturer’s recommended time, usually 30 seconds, to the occlusal surface, ensuring that all buccal and palatal fissures to be sealed are covered. The etching gel is available in syringes with a disposable cannula tip, which allows for accurate placing of the gel. Thirty-seven per cent phosphoric acid is normally used to create microporosities within the enamel, which permits a sealant to flow in and penetrate the etched surface, thereby producing a mechanical lock of resin tags.

Rinsing and drying the teeth

The tooth is fully washed for at least 20 seconds and dried for a minimum of 15 seconds, replacing wet isolation materials with dry ones. The tooth surface should be frosty white, and not shiny. If the tooth becomes wet by contamination from saliva, the etching procedure must be repeated.

Application of sealant

Sealant material is applied, allowing it to flow into the pits and fissures; this reduces the risk of air bubbles forming. Care should be taken to ensure that the pits and fissures are not overfilled. Occasionally the sealant material flows towards the distal surface of the tooth and a probe should be used to ensure that excess material is not left on this aspect as it could interfere with the occlusion or create an overhang, providing a susceptible site for dental caries to occur in the future.

Curing

The sealant should be cured for the manufacturer’s recommended curing time, usually between 20 and 30 seconds. A blue light source is used to cure the sealant material. A light-curing shield should also be used to protect the operator’s eyes.

Completion

All isolation materials should be removed and the tooth rinsed well. The surface of the sealant should be examined. A probe is used gently to ensure that all fissures are sealed and the tooth surface is smooth. A successful sealant feels hard and smooth without the presence of bubbles. The occlusion should be checked with articulating paper and any ‘high spots’ should be removed with a finishing bur or white stone as they will interfere with normal occlusion.

Review

The condition of sealants should be reviewed when patients attend for routine dental examinations. This step is crucial to the success and longevity of the material. The sealant should be checked for any loss of the material and also for any discolouration around the edges or underneath the sealant, which may be an indication of dental caries or partial debonding.

Fissure sealants are an effective preventive measure but should be used in conjunction with other preventive regimes, e.g. a low-cariogenic diet and fluoride therapy.

Fig. Part of the sealant has been lost and it should be repaired.

LOCAL ANAESTHESIA IN THERAPEUTIC DENTISTRY

 

Local anaesthetics provide temporary loss of sensation to a particular area of the mouth, so that the patient will not feel pain.

Techniques for local analgesia

The relevant anatomy and nerve supply of the oral region

In order to anaesthetise the teeth and oral mucosa for delivery of dental care the dental hygienist or therapist needs to be able to select and anaesthetise the sensory nerve supply. This is limited to two branches of the trigeminal nerve, i.e. the maxillary and mandibular divisions of the fifth cranial nerve. Brief summary of the branches and the structures supplied relevant to local analgesia of the maxillary and mandibular teeth is given in Tables 10.3 and 10.4.

 

The anatomy and distribution of  the trigeminal nerve – cranial nerve V

The trigeminal nerve is the main source of innervation for the oral cavity; it is the largest cranial nerve arising from the pons. At the semilunar ganglion, the trigeminal nerve divides into three divisions: the ophthalmic, the maxillary and the mandibular. It is the maxillary and mandibular divisions that innervate the teeth and their surrounding tissues.

Maxillary division

Fig. 5 The course and main branches of the maxillary division of

the trigeminal nerve.

 

The maxillary nerve leaves the cranium through the foramen rotundum and enters the pterygopalatine fossa where it subdivides into three main branches: the zygomatic nerve, the pterygopalatine nerves and the infraorbital nerve.

■ The zygomatic nerve enters the orbit through the inferior orbital fissure to supply sensory fibres to the zygomatic area of the face.

■ The pterygopalatine ganglion gives rise to the pterygopalatine nerves: the nasopalatine, the greater palatine and the lesser palatine nerve. They supply the sensory fibres to the palatal mucosa of the hard palate and palatal gingiva. The nasopalatine nerve passes through the incisive foramen to supply the anterior region and the greater palatine nerve passes through the greater palatine foramen to supply the posterior premolar and molar regions. The lesser palatine nerve passes through the lesser palatine foramen to supply the soft palate.

■ The infraorbital nerve enters the orbit through the inferior orbital fissure and passes along the infraorbital canal from where it finally emerges on to the face through the infraorbital foramen to supply the lower eyelid, the side of the nose and the upper lip. The infraorbital nerve gives off the superior alveolar nerve branches. These are:

► The posterior superior alveolar nerve: this branch is given off just before the infraorbital nerve enters the canal. It passes downwards on to the posterior surface of the maxilla and enters very small canals that run above the tooth roots to supply sensory fibres to the maxillary third and second molar teeth and the distobuccal and palatal roots of the maxillary first molar. This nerve also supplies sensory fibres to the adjacent buccal gingiva and maxillary sinus.

►The  middle superior alveolar nerve: this is not always present. When it is, it arises from the infraorbital nerve within the infraorbital canal. It passes down the wall of the maxillary sinus to supply sensory fibres to the mesiopalatal root of the maxillary first molar and the first and second premolar teeth. This nerve also supplies sensory fibres to the adjacent buccal gingiva and maxillary sinus.

► The  anterior superior alveolar nerve: this arises from the infraorbital nerve just before it emerges through the infraorbital foramen. It passes downwards inside the maxillary antrum. It supplies sensory fibres to the maxillary central and lateral incisor and canine teeth and to the adjacent labial gingiva. It also supplies the maxillary sinus.

The branches of the superior dental nerves form a plexus above the apices of the maxillary teeth.

Mandibular division

Fig. 6  The course and main branches of the mandibular division of

the trigeminal nerve. The fibres of the chorda tympani are shown in yellow.

 

The mandibular division is the largest division of the trigeminal nerve. It contains both motor and sensory fibres. It leaves the cranium through the foramen ovale and enters the infratemporal fossa (deep to the lateral pterygoid muscle), where it gives off the following branches:

■ Nerves to the muscles of mastication: these branches supply motor fibres to the masseter, temporalis and lateral pterygoid muscle.

■ Buccal nerve (long buccal): this nerve supplies sensory fibres to the mucosa and skin of the cheek and the buccal gingiva of the lower molar teeth.

■ Auriculotemporal nerve: this branch supplies sensory fibres to the temporomandibular joint, the skin of the outer ear and temporal area. It also carries parasympathetic fibres derived from the glossopharyngeal nerve to the parotid gland.

■ Lingual nerve: this branch supplies sensory fibres to the lingual gingiva of all the lower teeth, the anterior two thirds of the tongue and the floor of the mouth. The chorda tympani branch of the facial nerve joins the lingual nerve, providing special taste fibres to the anterior two thirds of the tongue. It also carries parasympathetic fibres to the submandibular ganglion to supply the submandibular and sublingual salivary glands.

■ Inferior dental (alveolar) nerve: this nerve enters the inferior dental canal through the mandibular foramen; just before it enters it gives off the mylohyoid nerve that supplies motor fibres to the mylohyoid muscle and the anterior belly of the digastric. Within the inferior dental canal, the inferior dental nerve gives off sensory fibres to the mandibular molars and premolars. At the mental foramen area the inferior dental nerve branches into the mental and incisive branch. The mental branch passes through the mental foramen to supply sensory fibres to the labial gingiva of mandibular anterior teeth, mucosa and skin of the lower lip and the chin. The incisive branch continues in the inferior dental canal to supply sensory fibres to the mandibular anterior teeth.

The mechanism of action of local analgesic agents

The other factor which determines efficacy of individual local analgesic agents is their effect on blood vessels. Those with a more effective vasoconstrictor property are retained at higher concentration for a longer period of time in the tissues; hence they provide better depth and duration of analgesia. The addition of a vasoconstrictor such as adrenaline (epinephrine) reduces local blood flow, slows down the rate of absorption of the local analgesic and thus prolongs the duration of analgesia. In dental formulations up to 1 in 80 000 adrenaline (12.5 µg/ml) is used in local analgesic solutions.

Lignocaine 2% with 1 in 80 000 adrenaline is a safe and effective formulation that has been used for routine dentistry for many years. In patients with severe hypertension or unstable cardiac rhythm the use of adrenaline in local analgesic solution is hazardous. In such patients it is usual to use prilocaine with or without felypressin (a vasoconstrictor related to octapressin). Both mepivacaine and articaine are available with and without adrenaline in their formulation.

Methods of application of local analgesic agents in dentistry

The methods currently available for delivering local dental analgesics are shown in Fig. 7, and these include:

■ Topical.

■ Jet.

■ Infiltration.

■ Regional block.

■ Intraosseous.

■ Intraligamentary.

Topical analgesia

Topical anaesthetics are used to reduce the sensation of needle penetration prior to local infiltration. There is little advantage to using topical agents when applying regional block analgesia. A variety of presentations for topical anaesthetic use is available, including:

The mucosa should be dried and topical agents left in contact with the tissues for a period of time as indicated by the manufacturer’s instructions. A new topical formulation designed to be placed as a gel into periodontal pockets is suggested for use in root surface instrumentation.

The gel preparation is easier to apply than sprays and can be more easily localised. Sprays can affect unwanted areas in the mouth and, because the taste may not be well tolerated by the patient, it should be sprayed on to cotton wool before placing in the mouth. Benzocaine gel is flavoured with attractive tastes, such as bubble gum, and so is more popular. Topical analgesics penetrate keratinised mucosa poorly. They are much more effective oon-keratinised mucosa. This means that they are less effective on palatal mucosa and attached gingivae. The topical analgesic should be applied to as small an area as possible. This reduces potential toxicity and prevents excessive numbness in the tongue and soft palate which may be unpleasant for the patient. Adequate time (approximately 2–3 minutes) should be allowed for the topical analgesic to take effect before embarking on infiltration analgesia.

Jet application

This method of application can be sufficient to be used  in isolation or can act to reduce the discomfort of subsequent injection of local analgesic. Jet application works by forcing analgesic through the oral mucosa under high pressure. Most systems use conventional liquid, but powder applications are in use. Disadvantages include haematoma formation and an unpleasant taste should the solution be spilled into the mouth.

Infiltration analgesia

Using modern local analgesic preparations, infiltration is a simple technique. The agent is deposited beneath the epithelium but above the periosteum within the mucosa. The analgesic is deposited around the terminal nerve endings and is therefore effective in a given site regardless of the source of the innervation. In the maxilla, the cortical bone is thinner than in the mandible, and simple buccal infiltration can deliver pulpal analgesia (Fig. 8). The ideal application is for a local site which is free from infection. Infection may be spread by injecting into the site and reduces the efficacy of analgesia. In the mandible, with the exception of the incisor teeth, the thick cortical layer of bone present prevents the use of an infiltration technique for molar analgesia in the adult dentition. The needle should be introduced in the buccal fold within the reflected mucosa. By stretching the tissues, smooth penetration of the needle with minimal discomfort is assured. Injection into the epithelium produces blistering and pain, so the needle should be advanced into the mucosa before injection starts. Injection beneath the periosteum is painful and produces postanalgesic discomfort. Aspiration should be performed before injecting. A slow injection rate of 1 ml over 30 seconds is ideal. The technique takes approximately 2 minutes before analgesia is achieved. Pulpal analgesia lasts for 45 minutes (2% lignocaine with 1:80 000 adrenaline), soft tissue analgesia lasts for a longer duration; approximately 1–2 ml of solution should be injected. Occasionally there is an additional nerve supply in the maxilla to pulpal tissue from the greater palatine and nasopalatine nerves. In this case an additional palatal infiltration is required. The upper first molar has a nerve supply from both the posterior and middle superior alveolar nerves and, given that buccal access may be reduced due to the zygomatic buttress, a block of these nerves may be required as infiltration will be ineffective. Palatal infiltration (Fig. 9) can be used to anaesthetise palatal soft tissue for upper teeth distal to the canine. The injection should be placed just distal to the selected tooth, 10–15 mm from the gingival margin. Only a few drops of solution are required.

Figure 8. The use of infiltration technique demonstrated on a maxillary skull.

Figure 9. Ideal palatal injection site.

Intraosseous analgesia

When infiltration is not effective, intraosseous delivery can be useful. The technique relies upon the deposition of analgesic solution directly into cancellous bone. Following infiltration of the attached gingiva, a slow-speed drill is used to perforate the buccal plate of bone at an interdental location. Next a 6 mm, 27 gauge needle is used to deliver 1 ml of solution over a 2-minute period. Although requiring a smaller dose of analgesic, the technique is unsuitable for teeth with periodontal disease, in the presence of limited attached gingiva or limited interradicular bone.

Disadvantages of the technique which include:

■ Specialist equipment required.

■ Teeth may be damaged.

■ Increased risk of systemic toxicity.

■ Technically more demanding than infiltration analgesia.

 Intraligamentary analgesia

This method delivers analgesic by injection into the periodontal ligament. The solution then enters cancellous bone through perforations in the tooth socket wall rather than by moving down the length of the periodontal ligament to reach apical nerve fibres. Specialist equipment with a 30 gauge needle is available.

The technique produces bacteraemia and poses an increased risk of systemic effects. There is a risk of inducing periodontal damage or infection resulting in pain following injection. Although contraindicated in the presence of active periodontal disease, the technique can be used to avoid the need for inferior dental block in children and to treat patients with bleeding disorders without the need for provision of blood clotting factors.

Regional block analgesia

The delivery of regional block analgesia in the maxilla is not permitted by the dental hygienist or dental therapist. The technique which deposits analgesic at the nerve trunk poses an increased risk of direct trauma to the nerve, haemorrhage and intravascular injection of solution. Given the success of infiltration techniques, the dental hygienist or therapist will rarely have difficulty in delivering painless dental care using infiltration methods alone in the maxilla.

In the mandible, the choice of technique for analgesia delivery is dependent upon the age of the patient and the location of the tooth to be anaesthetised. Infiltration is successful in obtaining analgesia for mandibular primary teeth. In adults infiltration is preferable to regional block for pulpal analgesia of the mandibular incisor teeth due to its efficacy and as a result of supply from the contralateral inferior dental nerve to central incisor teeth.

Regional block methods in the mandible will produce a widespread area of analgesia from a single injection and have the advantage that the delivery of analgesic is at sites discrete from local areas of infection.

                               

Fig.10  Method of inferior alveolar dental nerve anaesthesia.                           Fig. 11  Direct method of inferior alveolar dental nerve block.

 

Regional block analgesia has the following disadvantages:

■ The technique is more difficult than infiltration.

■ Midline crossover of nerve supply is not managed.

■ Patients dislike the excessively wide distribution of soft tissue analgesia.

■ Deep tissue haemorrhage can cause infection and trismus.

■ Although rare, direct nerve injury may occur.

Regional block applications in the mandible include:

■ Inferior alveolar and lingual nerve block.

■ Incisive and mental nerve block.

■ Long buccal nerve block.

■ Mylohyoid nerve block.

The dental hygienist and dental therapist are trained to deliver the inferior alveolar nerve block as a means of securing pulpal analgesia in adult mandibular canines, premolar and molar teeth. The technique aims to deposit local analgesic solution in close proximity to the mandibular foramen on the medial aspect of the mandibular ramus. The analgesic solution thus blocks nerve conduction where the nerve is accessible before it enters the inferior alveolar canal.

The direct technique uses simple anatomical landmarks to assist the operator in locating the mandibular foramen. The patient’s mouth is opened wide and the ramus is held with the thumb on the retromolar area in the coronoid notch of the ascending ramus. The thumb palpates the internal oblique ridge of the mandible and stretches the overlying mucosal thus facilitating easy needle penetration. The index finger is placed exteriorly on the posterior aspect of the ramus at the same height as the thumb. In the adult the mandibular foramen is halfway between the operator’s thumb and index finger. The syringe is placed across the premolars of the opposite side of the mouth and directed between the external oblique ridge and the pterygomandibular raphe. The technique is not always successful. Failure may be due to faulty technique, anatomical variation in the location of the mandibular foramen, bending of the needle or accessory nerve supplies.

DIFFICULTIES, COMPLICATIONS AND EMERGENCIES WHICH CAN BE ASSOCIATED WITH LOCAL ANALGESIA

Despite the recognition that local analgesia has a safe record in dental applications, it is important to be familiar with potential complications. At greatest risk of complication from use of local analgesia are children, the elderly and the medically compromised. It is vital to obtain a careful medical history including analgesic history before delivering local analgesic, since allergy, toxicity and drug interactions account for the most serious complications.

Adverse effects of local analgesics include:

■ Trauma.

■ Failure to achieve analgesia.

■ Toxicity.

■ Fainting.

■ Hypersensitivity.

■ Drug interactions.

■ Facial nerve paralysis.

Trauma

The delivery of rapid injection or poor technique can result in direct nerve damage or haematoma formation. These can lead to pain and patient anxiety. Pain at the time of injection can be avoided by careful technique, including the use of a slow injection of isotonic solution. After-pain results from direct tissue trauma resulting in haematoma, infection or trismus.

 Failure to achieve analgesia

Patient anxiety may lead not only to fainting but also to a reduced analgesic efficacy. In such cases it may be necessary to consider the use of conscious sedation to reduce anxiety. Provided they have had appropriate training, a dental hygienist or therapist may treat patients who are sedated in this way but only if a dental surgeon is present in the surgery. Inflammation in the site of injection will prevent adequate analgesia. In such circumstances, use of a regional block may be more successful. Anatomical variation in relation to bone architecture and nerve supply also accounts for failure to achieve analgesia.

 Fainting

Fainting may occur before, during or after the administration of local analgesic. Typically the patient will become pale, sweaty and complain of nausea. Some patients describe a tingling sensation in the hands and feet prior to loss of consciousness; the pulse is first rapid then becomes slow and weak. Fainting is due to a reduction in cranial blood supply subsequent to a slowing of the heartbeat due to intense vagal stimulation. Fainting can be avoided by dealing with the patient in a calm, reassuring and confident manner. The delivery of local analgesia should always take place with the patient in a supine position. In the event of a faint, lay the dental chair flat to ensure a supply of blood to the brain. The patient should recover spontaneously and treatment can then continue.

INSTRUMENTS USED IN DENTAL LOCAL ANALGESIA

Name Self-aspirating local anaesthetic syringe Function and features • Used to administer local anaesthetic with a disposable anaesthetic cartridge and a disposable needle • The finger bar of the syringe controls the piston rod, which depresses the rubber stopper of the anaesthetic cartridge during aspiration •When the piston rod is depressed, the local anaesthetic solution is forced out through the disposable needle, which is screwed onto the threaded tip • The barrel of the syringe is open on both sides to facilitate loading the anaesthetic cartridge and check for blood cells during aspiration Variations Non-self-aspirating type, disposable type (assembled), top loading type, intraligamentary syringe	Name Disposable needle Function, features and precautions • Used in conjunction with a self-aspirating local anaesthetic syringe and disposable local anaesthetic cartridge • Is threaded onto the hub of syringe – the short end of needle punctures the rubber diaphragm of the cartridge • Single use • Disposed of in the sharps’ container • Prior to use, check: seal is intact, expiry date and the length and gauge of the needle • Lumen is the hollow centre of the needle •Gauge is the thickness of the needle •The type of injection dictates the appropriate length and gauge of needle to be used Varieties Available in different lengths and gauges	Name Glass disposable local anaesthetic cartridge Function, precautions and contents • Contains local anaesthetic solution for delivery • Prior to use check: expiry date, cartridge and rubber diaphragm are intact and the colour of the local anaesthetic solution • Single use • Disposed in the sharps’ container • Contains water, preservatives, anaesthetic solution and buffering agents; some contain vasoconstrictors Varieties • Local anaesthetic constituents may vary • May be presented in a plastic cartridge

 

Syringes, along with attached needles and analgesic cartridges, are required for conventional delivery of local analgesic with simple hand pressure. Computerised delivery systems have a pump to control the pressure and hence the rate of injection. Current safe policy for the use of used needles precludes re-sheathing. Modern disposable syringe and needle combinations avoid the need to dismantle or re-sheath used needles, thereby reducing the risk of sharps injuries.

Needles for use with dental syringes have a stainless steel silicon tip with a bevelled edge and a plastic hub. Specialist dental needles have a portion adjacent to the but which protrudes. Standard Luer type needles are used in some systems. Luer type needles are supplied in sterile blister packs, whereas dental needles are supplied with individual sterile sheaths with seals indicating the needle size and date up to which the contents are sterile. If the seal is damaged the needle should be discarded. Primarily, needles are supplied in varying lengths and two gauges. The gauge measures the external diameter of the needle. The 30 gauge needle is 0.3 mm and the 27 gauge is 0.4 mm diameter. The length of needles ranges from 9 to 14 mm. All dental needles are disposable single use; they should never be bent to improve access as this poses the risk of needle fracture.

Dental analgesic cartridges have three components:

■ Cylinder.

■ Plunger.

■ Cap.

The cylinder has information stamped on it indicating the contents, concentrations and expiry date, along with the manufacturer’s name and batch number. Glass cylinders can be used for all dental applications. Plastic cylinders are produced but are not suitable for use in intraligamentary equipment. Before using a local analgesic cartridge the operator must confirm the drug and concentration present and check that the expiry date has not passed. The contents should be checked, to ensure there is no clouding of contents, large air bubbles, cracks or disturbance of the plunger. The plunger is composed of rubber, although constituents do vary and some products contain latex. Both solid and hollow plungers are used in dental cartridges. Hollow plungers are designed to work with self-aspirating syringe systems.

The syringes for use in local analgesia are designed for specific applications including:

■ Conventional.

■ Intraligamentary.

■ Power injectors.

■ Computerised.

Conventional syringes for dental analgesia are made of metal or alternatively from disposable plastic. Reusable metal components should withstand sterilisation without sustaining damage. Although individual manufacturers’ products do vary, the general design is composed of:

■ A barrel.

■ A viewing point.

■ A threaded needle-mounting hub.

■ A plunger rod.

■ A handle or thumb ring or rest.

■ Finger grips.

Aspiration

In order to avoid accidental intravascular deposition of analgesic solution, it is necessary to routinely aspirate before injecting. Non-aspirating syringes are not recommended for dental use as it is not possible to determine if the tip of the needle is in a vein. If an artery has been entered then simply removing the pressure will allow some blood to flow into the cartridge. However, this is a rare event and the risk is greater of accidental intravenous penetration. Positive aspiration systems require the operator actively to apply negative pressure. A plunger hook or barbed plunger tip allows the plunger rod tip to engage the plunger rod. Pulling back the rod withdraws the plunger, thereby reducing the pressure in the cartridge. The technique is prone to error. In applying negative pressure the tip of the needle tends to move such that the site of aspiration may not correspond to the site of injection. Passive aspiration is a superior system as it requires only minimal movement of the operator’s thumb. An aspirating nipple is designed within the plunger such that, provided pressure is simply released, a negative pressure is produced within the cartridge; if the needle tip is within a blood vessel this will be evident because of the presence of blood visible within the cartridge.

Information was prepared by Levkiv M.O.