5. Post-eruptive un-carious lesions of teeth.  Pathomorphology, clinic, diagnosis and treatment of un-carious lesions.

 

Classification of un-carious lesions:

I. Lesions that occur in the stage of dental follicle development, before eruption:

         1. hypoplasia;

         2. hyperplasia of enamel (enamel pearls);

         3. endemic fluorosis;

         4. disorders of development and eruption;

         5. genetic disturbances of tooth development.

II. Lesions that occur after teeth have been erupted:

         1. tooth wear: attrition, abrasion, wedge-shaped defect;

         2. erosion;

         3. necrosis of hard tooth tissues;

         4. hyperesthesia;

         5. trauma of teeth;

         6. fluorosis;

 

Tooth wear

Tooth wear is defined as loss of tooth tissue due to causes other than caries. Some tooth wear is normal and occurs with age. This is termed physiological tooth wear. However, excessive tooth wear is pathological. Three types have been described: attrition, abrasion and erosion. Although these may occur separately, in many instances they occur together.

Attrition

Attrition  is  the  process  of  wearing  away  of  enamel,  which  occurs physiologically as a consequence of mastication. This process is very slow and results in  a  gradual  loss  of  enamel.  Pindborg  disitinguished  three  types  of attrition: physiological, excessive and pathological. The dental pulp cavity is usually not open due to attrition.

 

Fig.   Attrition.

This patient has marked attrition of the occlusal surfaces of most of his teeth.

 

Attrition is tooth wear caused by tooth-to-tooth contact. It occurs as a normal part of ageing and it is usually the incisal edges which wear away first, followed by the occlusal surfaces of the molar teeth. There may also be loss of interproximal tooth tissue leading to mesial migration of the teeth. Excessive occlusal wear may occur in the following situations:

■ Patients with bruxism. These patients grind their teeth excessively and in some cases this is triggered by occlusal irregularities.

■ Patients who have lost several posterior teeth may show excessive attrition of the anterior teeth, especially if these are used for chewing.

■ Patients who suffer from developmental disturbances of tooth structure, such as amelogenesis and dentinogenesis imperfecta, may suffer exceptional tooth wear.

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Fig. Attrition: mandibular incisor teeth with enamel worn away thus exposing the brown discolored dentin.

 

Abrasion

Abrasion is frictional tooth loss caused by extrinsic agents. It is always pathological and may be caused by tooth brushing and habits such as biting on a pipe or a pencil. Tooth brush abrasion is characteristic and is caused by poor tooth brushing technique, i.e. patients brushing horizontally with excessive force. It has the  following characteristics:

It particularly affects the labial and buccal surfaces of the upper incisor, canine and premolar teeth.

The resulting cavity is wedge-shaped with a sharp angle towards the occlusal surface and an obtuse angle towards the apical surface.

The problem is often compounded by the use of hard tooth brushes and abrasive tooth paste.

Fig. Erosive-abrasive defect in the upper jaw involving all teeth except for tooth 16.

 

Abrasion is defined as a defect of hard dental tissues caused by the mechanical action of abrasives on the tooth surface. It is found most frequently in the region of the tooth cervix as a wedge-shaped defect. The loss of both dentin and enamel  is  present. 

 

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Fig. Wedge-shaped defect

These  wedge-shaped defects  can  lead  to  the  denudation  of dental pulp. At the beginning, the smooth walls of the defect are very sensitive to various  (mechanical,  chemical  or  physical)  stimuli  but  later  this  sensitivity descreases. Wedge-shaped defects are usually to be one of the characteristic symptoms of chronic generalized periodontitis.

 

Erosion

Erosion is the loss of tooth substance caused by chemical agents and is non-bacterial and therefore does not include loss by caries. Most erosion is caused by acids and is seen in the following groups:

Those with gastric reflux and with bulimia and anorexia. Regurgitation of acid from the stomach  particularly affects the palatal surfaces of the upper maxillary teeth.

As an occupational hazard. Those who work in an acidic environment, e.g. in factories making batteries, and also in wine tasters. Erosion in these groups is relatively rare but because the acid is in the environment the erosion is particularly seen on the labial surfaces of both the upper and lower incisor teeth.

Those who consume excessive amounts of carbonated soft drinks or fruit juices. This group is by far the largest and in the Western world it is particularly children, adolescents and young adults who are affected.

The surfaces which are most commonly affected are the palatal surfaces of the upper anterior teeth. The teeth may appear yellow due to the reduction in the thickness of the enamel and typically the cavities are shallow and broad. Patients with erosion may be unaware that they have a problem but others may complain of sensitivity, particularly on eating hot and cold foods.

                                                        Fig. Erosion: buccal surfaces of right maxillary cuspid  and  first  premolar  tooth  showing  loss  of  enamel.

Both central and right lateral incisor teeth show white areas at their labial surfaces indicating incipient

decalcification but still maintaining their crystalline structure

 

There is no doubt, the process of tooth wear is often the combination of two or all three factors and those that are more likely to occur are erosion and attrition.

Acids in the mouth cause the surface of the tooth to be weakened which allows tooth-to-tooth contact during mastication to effect greater loss of the tooth surface than would otherwise be the case if erosion or attrition were occurring alone. The source of the acid may be intrinsic, arising from gastric acid escaping from the stomach into the oesophagus and then into the mouth. This may be a result of a weakened or defective sphincter between the stomach and oesophagus leading to gastro-oesophageal reflux disease (GORD) with usually accompanying indigestion, heartburn and epigastric pain as well as dental erosion. Recurrent vomiting also has similar effects and this may be associated with irritable bowel syndrome or travel sickness, or it may be self-induced as occurs in the eating disorders of anorexia and  bulimia nervosa. Extrinsic acids arise from dietary sources and whilst carbonated drinks and fruit juices are readily identified as being the cause, it should also be remembered that foods such as pickled vegetables, brown sauce and tomato ketchup do have erosive potential.

This erosion can affect any surface which comes into contact with the acid but it is more likely to occur on the occlusal and palatal surfaces of the maxillary teeth and to a lesser extent of the mandibular teeth.

Fig. 12.9 shows severe tooth surface loss as a result of excessive intake of carbonated drinks. The considerable erosion that has taken place is well demonstrated by the raised appearance of the amalgam restoration on the palatal surface of the maxillary right lateral incisor. The amalgam at the time of placement was flush with the enamel surface but now the latter is well below the original level. Fig. 12.10 shows erosion as a result of gastro-oesophageal reflux disease.

It is important that the condition is recognised at an early stage when the aetiological factors may be identified. Where it is dietary in origin, diet analysis and counselling will prevent further deterioration in the condition. Patients with gastro-oesophageal reflux disease or eating disorders should be referred initially to their medical practitioner. Where the amount of tooth loss has been mild and in the absence of tooth sensitivity, the condition may be left and the situation monitored at regular intervals to ensure that the wear has stopped. Where there has been a greater degree of surface loss, then restorative treatment by way of composite coatings, veneers or crowns may be required.

The method of erosion and abrasion (cervical lesions) treatment is as follows:

■ Access: this is not normally difficult unless the lesion is on the lingual surface of a molar tooth. The amount of cavity preparation depends on the cause of the lesion: abrasion and erosion lesions may only require the cutting of a bevel and cleaning of the cavity with a pumice and water paste, whereas carious cavities may require access with a high-speed round diamond bur and caries removal with an excavator or round stain-less steel slow-speed bur.

■ Material placement: resin composite is generally the material of choice for such restorations but amalgam may be placed in posterior teeth; in difficult, subgingival cavities glass ionomer-based materials may be used. Glass ionomers should be protected with either varnish or an unfilled resin for the first few days after placement to protect them from moisture contamination. The material may be shaped free-hand or with a matrix.

Clinical significance

It is important to recognize that excessive tooth wear is taking place and to diagnose the most likely cause. In many cases the causes may be multiple. Abrasion caused by tooth brushing may be reduced by improving brushing technique. A careful history and detailed notes on the position of the erosion are important in order to determine the precise cause. Dietary analysis and advice are essential for those suffering from erosion due to dietary causes.

 

Fluorosis

In the case of excessive consumption of fluorine one can consider fluorosis to be un-carious lesion that occurs after teeth has been erupted. In endemic regions, fluorosis  is considered to be an un-carious lesion that occur before teeth eruption, on the stage of dental follicle formation (for temporary dentition it is 4-5 m of intrauterine life, for permanent dentition it is 4-10 m of life).

Fig. Dental fluorosis. The abnormalities may vary from moderate (a) to severe (b). Enamel shows white spots,

brown discolorations, and surface irregularities indicating both enamel hypocalcification and hypomineralisation.

 

Over the last fifteen years it has been noted that an increasing number of infants and very young children have tended to swallow some of the tooth-paste used, and this is likely contributing to the increasing level of enamel fluorosis. Also, a pea-sized amount of toothpaste on the brush is more than adequate to clean young children’s teeth, but this amount (0.25–0.3 g) is often exceeded. Enamel fluorosis is a risk if too much fluoride toothpaste is used at too young an age and at too high a concentration.

Fluoride Supplements

Fluoride supplements are a risk factor for fluorosis in young children when used inappropriately and when not conforming to appropriate dosing schedules. Many studies have reported a clear association between supplement use by children aged less than 6 years and enamel fluorosis. Fluoride supplements can be prescribed for children at high risk of dental caries. When  considering the prescription of fluoride supplements for children less than 6 years, dentists should weigh the risk for caries without fluoride supplements, the caries prevention offered by supplements and the potential for enamel fluorosis.

Risk Management for Enamel Fluorosis

A major risk factor in enamel fluorosis is inappropriate use of fluoride toothpaste at a young age. Use of fluoride toothpaste should continue due to the additive benefit from the combination of fluoridated water and toothpaste. The Forum on Fluoridation1 2002 recommends that parents should be advised to use a toothbrush and water to brush the teeth of children less than 2 years of age. Parents should consult professional advice with regard to the use of fluoride toothpaste when children are perceived to be at a high risk of dental decay. Children aged between 2–7 years of age should be supervised when brushing, using only a pea-sized amount of toothpaste and should also be encouraged to expectorate excess. The use of paediatric toothpastes with low concentrations of fluoride requires further research before they can be recommended. Having reviewed data from more recent studies were found that little decline in caries levels was observed between 0.7 and 1.2 ppm fluoride in water, while an increase in fluorosis was seen at this level. The authors suggested that a suitable trade-off between dental decay and fluorosis appears to occur at 0.7 ppm.

 

It is important to consider calcification and eruption dates of permanent teeth in order to identify when developing teeth are at most risk of enamel fluorosis (Tables 1 and 2). The occurrence of enamel fluorosis is strongly associated with cumulative fluoride ingestion during enamel development, but the severity of the condition depends on the dose, timing and duration of the fluoride intake. Permanent incisors begin calcifying at 3–4 months, and this is completed at 4–5 years (Table 2, Berkowitz et al. 1992).

The first year of life was the most critical period for developing fluorosis on aesthetically important maxillary central incisors. However, the greatest risk of fluorosis was associated with a four-month critical period starting at 22 months after birth. A more recent study showed that the first 3 years were the critical period for fluorosis on maxillary central incisors.

Table 1.

        

Table 2.

 

Acceptable measures of fluorine in water according to hygienic standards is 0,8-1,2(1,5) mg/l. Fluorosis is the term given to changes in the enamel which are associated with excess ingestion of fluoride. These vary from localised white opacities to more severe brown–yellow mottling on the teeth. The precise effect depends on the dose of fluoride (from all sources), the duration for which it was taken and the age of the patient at the time of ingestion. Fluorosis when very severe (concentrations in the water supply greater than six parts per million) may result in extensive hypoplasia with brown staining.

Fluoride toxicity

Excessive ingestion of fluoride can result in fluorosis (mottling) which presents as opaque or white areas, lines or flecks in the enamel surface and can be cosmetically disfiguring when they occur on anterior teeth. Fluorosis can occur at different times and varies in severity. Fig. 11.2 shows very mild dental fluorosis (graded TF1) and Fig. 11.3 shows more severe fluorosis (graded TF3), classified by the York Review as being ‘of aesthetic concern’. The most important time is when ingestion of excessive fluoride occurs during enamel formation of the aesthetically important permanent upper anterior teeth at between 15 and 30 months of age, although this period can be extended from birth to 6 years.

More severe and cosmetically unacceptable cases of fluorosis are uncommon in the UK but these can result from the use of fluoride supplements in areas where the water is artificially fluoridated or where fluoride occurs naturally at the optimum level of 1 ppm.

 

It has been estimated that about 20% of all enamel defects in the UK are attributable to fluorosis but mainly of the mildest form (TF1). Most of the staining in mottled enamel is confined to the outer 50–100 µm, so if treatment is considered necessary this is usually by composite restorations or in severe cases (Fig.11.4) by crowning or veneers.

More severe toxicity can result in systemic disease such as osteoporosis and skeletal deformity (Table 11.3).

 

TRAUMA

Trauma to the oral region occurs frequently and comprises 5% of all injuries for which people seek treatment. In preschool children the figure is as high as 18% of all injuries. Amongst all facial injuries, dental injuries are the most common of which crown fractures and luxations occur most frequently. An appropriate treatment plan after an injury is important for a good prognosis. Guidelines are useful for dentists and other health care professionals in delivering the best care possible in an efficient manner. The International Association of Dental Traumatology (IADT) has developed a consensus statement after a review of the dental literature and group discussions. The first set of guidelines was published by IADT in 2001. Experienced researchers and clinicians from various specialties were included in the group. In cases where the data did not appear conclusive, recommendations were based on the consensus opinion of the IADT board members. The guidelines represent the current best evidence, based on literature research and professional opinion. As is true for all guidelines, the health care provider must apply clinical judgment dictated by the conditions present in the given traumatic situation. The IADT does not guarantee favorable outcomes from following the Guidelines, but using the recommended procedures can maximize the chances of success. Because management of permanent and primary dentition differs significantly.

 

Uncomplicated crown fracture

Fracture involves enamel or dentin and enamel; the pulp is not exposed.  Sensibility testing may be negative initially indicating transient pulpal damage; monitor pulpal response until a definitive pulpal diagnosis can be made.

Treatment: If tooth fragment is available, it can be bonded to the tooth. Urgent care option is to cover the exposed dentin with a material such as glass ionomer or a permanent restoration using a bonding agent and composite resin. Definitive treatment for the fractured crown may be restoration with accepted dental restorative materials

 

Complicated crown fracture

Fracture involves enamel and dentin and the pulp is exposed. Sensibility testing is usually not indicated initially since vitality of the pulp can be visualized. Follow up control visits after initial treatment includes sensibility testing to monitor pulpal status.

Treatment: In young patients with immature, still developing teeth, it is advantageous to preserve pulp vitality by pulp capping or partial pulpotomy. This treatment is also the choice in young patients with completely formed teeth. Calcium hydroxide and MTA (white) are suitable materials for such procedures.

 In older patients, root canal treatment can be the treatment of choice, although pulp capping or partial pulpotomy may also be selected. If too much time elapses between accident and treatment and the pulp becomes necrotic, root canal treatment is indicated to preserve the tooth. In extensive crown fractures a decision must be made whether treatment other than extraction is feasible.

 

Crown-root fracture

Fracture involves enamel, dentin and root structure; the pulp may or may not be exposed. Additional findings may include loose, but still attached, segments of the tooth. Sensibility testing is usually positive.

Treatment: Treatment recommendations are the same as for complicated crown fractures (see above). In addition, attempts at stabilizing loose segments of the tooth  by bonding may be advantageous, at least as a temporary measure, until a definitive treatment plan can be formulated

 

Root fracture

The coronal segment may be mobile and may be displaced. The tooth may be tender to percussion. Sensibility testing may give negative results initially, indicating transient or permanent pulpal damage; monitoring the status of the pulp is recommended. Transient crown discoloration (red or grey) may occur

Treatment: Reposition, if displaced, the coronal segment of the tooth as soon as possible. Check position radio graphically. Stabilize the tooth with a flexible splint for 4 weeks. If the root fracture is near the cervical area of the tooth, stabilization is beneficial for a longer period of time (up to 4 months).

 It is advisable to monitor healing for at least 1 year to determine pulpal status. If pulp necrosis develops, root canal treatment of the coronal tooth segment to the fracture line is indicated to preserve the tooth.

Information was prepared by Levkiv M.O.