Regressive Alterations of the Teeth
Regressive changes in the dental tissues include a variety of alterations that are not necessarily related either etiologically or pathogenetically. Some of the changes to be considered here are associated with the general aging process of the individual. Others arise as a result of injury to the tissues. Still other regressive changes of teeth occur with such frequency that there is some doubt whether they should actually be considered pathologic. None of the lesions discussed here can be regarded as developmental abnormalities or as inflammatory lesions. They are brought together in this chapter because they do represent what must be considered lesions of a retrograde nature.
Mechanical wear and tear of tooth substance is a consequence of both physiological and pathological means and therefore different adaptive strategies have evolved to tackle this situation. A disease state arises when this delicate balance goes awry resulting in early dissolution and loss of tooth substance with subsequent involvement of pulpal and periapical tissues. It is currently acknowledged that there are several mechanisms that contribute to tooth wear. These include abrasion resulting from the friction of exogenous material forced over tooth surfaces (e.g. masticating food) or the use of teeth as ‘tools’, erosion resulting from the chemical dissolution of tooth surfaces (e.g. effects of acid from various sources or from a highly acidic diet), and attrition from tooth-to-tooth contact (e.g. night grinding). These mechanisms most often occur together, each acting at different intensity and duration in a continuously changing salivary medium, producing immensely variable patterns and degrees of wear.
Attrition may be defined as the physiologic wearing away of a tooth as a result of tooth-to-tooth contact, as in mastication. This occurs only on the occlusal, incisal, and proximal surfaces of teeth, not on other surfaces unless a very unusual occlusal relation or malocclusion exists. This phenomenon is physiologic rather than pathologic, and it is associated with the aging process. The older a person becomes, the more attrition is exhibited.
Attrition commences at the time contact or occlusion occurs between adjacent or opposing teeth. It may be seen in the deciduous dentition as well as in the permanent, but severe attrition is seldom seen in primary teeth because they are not retained normally for any great period of time. Occasionally; however, children may suffer from either dentinogenesis imperfecta or amelogenesis imperfecta, and in both diseases pronounced attrition may result from ordinary masticatory stresses.
The first clinical manifestation of attrition may be the appearance of a small polished facet on a cusp tip or ridge or a slight flattening of an incisal edge. Because of the slight mobility of the teeth in their sockets, a manifestation of the resiliency of the periodontal ligament, similar facets occur at the contact points on the proximal surfaces of the teeth. As the person becomes older and the wear continues, there is gradual reduction in cusp height and consequent flattening of the occlusal inclined planes. According to Robinson and his associates, there is also shortening of the length of the dental arch due to reduction in the mesiodistal diameters of the teeth through proximal attrition.
Only minor variation in the hardness of tooth enamel exists between individuals; nevertheless considerable variation in the degree of attrition is observed clinically. Men usually exhibit more severe attrition than women of comparable age, probably as a result of the greater masticatory force of men. Variation also may be a result of differences in the coarseness of the diet or of habits such as chewing tobacco or bruxism either of which would predispose to more rapid attrition. Certain occupations, in which the person is exposed to an atmosphere of abrasive dust and cannot avoid getting the material into his/ her mouth, also are important in the etiology of severe attrition.
Advanced attrition, in which the enamel has been completely worn away in one or more areas, sometimes results in an extrinsic yellow or brown staining of the exposed dentin from food or tobacco (Figs. 13-1, 13-2). Provided there is no premature loss of the teeth, attrition may progress to the point of complete loss of cuspal interdigitation. In some cases the teeth may be worn down nearly to the gingiva, but this extreme degree is unusual even in elderly persons.
The exposure of dentinal tubules and the subsequent irritation of odontoblastic processes result in formation of secondary dentin (q.v.) pulpal to the primary dentin, and this serves as an aid to protect the pulp from further injury. The rate of secondary dentin deposition is usually sufficient to preclude the possibility of pulp exposure through attrition alone. Sometimes, as the teeth wear down by attrition, little tendrils of pulp horn remain and are exposed to the oral cavity. These can be seen only when the tooth is examined carefully under a magnifying lens.
Abrasion is the pathologic wearing away of tooth substance through some abnormal mechanical process. Abrasion usually occurs on the exposed root surfaces of teeth, but under certain circumstances it may be seen elsewhere, such as on incisal or proximal surfaces.
Robinson stated that the most common cause of abrasion of root surfaces is the use of an abrasive dentifrice. Although modern dentifrices are not sufficiently abrasive to damage intact enamel severely, they can cause remarkable wear of cementum and dentin if the toothbrush carrying the dentifrice is injudiciously used, particularly in a horizontal rather than vertical direction. In such cases abrasion caused by a dentifrice manifests itself usually as a V-shaped or wedge-shaped ditch on the root side of the cementoenamel junction in teeth with some gingival recession (Fig. 13-3). The angle formed in the depth of the lesion, as well as that at the enamel edge, is a rather sharp one, and the exposed dentin appears highly polished. It has been shown by Kitchin and by Ervin and Bucher that some degree of tooth root exposure is a common clinical finding, and a 66% incidence of abrasion among 1,252 patients examined was reported by Ervin and Bucher. The fact that abrasion was more common on the left side of the mouth in right-handed people, and vice versa, suggested that improper toothbrushing caused abrasion. The results of a study by the American Dental Association on the comparative abrasiveness of a number of popular dentifrices are shown in Table 13-1 and indicate the wide variation among the commercial products.
|T-Lak||Laboratories Cazé||20 (20–21)+ (Lowest)|
|Thermodent||Chas. Pfizer & Co.||24 (23–24)|
|Listerine||Warner-Lambert Pharm. Co.||26 (22–30)|
|Pepsodent*||Lever Brothers Co.||26 (23–29)|
|Amm-i-dent||Block Drug Co.||33 (31–34)|
|Colgate with MFP||Colgate-Palmolive Co.||51 (46–56)|
|Ultra-Brite||Colgate-Palmolive Co.||64 (52–82)|
|Macleans,* Spearmint||Beecham Inc.||66 (66)|
|Macleans,* regular||Beecham Inc.||70 (68–72)|
|Pearl Drops||Cameo Chemicals||72 (65–83)|
|Crest, mint*||Procter & Gamble Co.||81 (71–90)|
|Close-up||Lever Brothers Co.||87 (70–101)|
|Macleans, Spearmint||Beecham Inc.||93 (85–99)|
|Macleans, regular||Beecham Inc.||93 (74–103)|
|Crest, regular*||Procter & Gamble Co.||95 (77–110)|
|Gleem||Procter & Gamble Co.||106 (88–136)|
|Phillips||Sterling Drug Inc.||114 (111–116)|
|Vote||Bristol-Myers Co.||134 (112–162)|
|Sensodyne||Block Drug Co., Inc.||157 (151–168)|
|Iodent No. 2||Iodent Co.||174 (172–176)|
|Smokers toothpaste||Walgreen Lab., Inc.||202 (198–205) (Highest)|
Modified from American Dental Association Report of the Council on Dental Therapeutics: Abrasivity of current dentifrices. J Am Dent Assoc, 81:1177, 1970. Copyright by the American Dental Association. Reprinted by permission.
Other less common forms of abrasion may be related to habit or to the occupation of the patient. The habitual opening of bobby pins with the teeth may result in a notching of the incisal edge of one maxillary central incisor (Fig. 13-4). Similar notching may be noted in carpenters, shoemakers, or tailors who hold nails, tacks, or pins between their teeth. Habitual pipe smokers may develop notching of the teeth that conforms to the shape of the pipe stem (Fig. 13-5). The improper use of dental floss and toothpicks may produce lesions on the proximal exposed root surface, which also should be considered a form of abrasion.
It is apparent that though the etiology of abrasion can be varied, the pathogenesis under these different conditions is essentially identical. The loss of tooth substance that occurs by one means or another is certainly pathologic but should present no problem in diagnosis.
The exposure of dentinal tubules and the consequent irritation of the odontoblastic processes stimulate the formation of secondary dentin similar to that seen in cases of attrition. Unless the form of abrasion is an extremely severe and rapidly progressive one, the rate of secondary dentin formation is usually sufficient to protect the tooth against pulp exposure.
Dental erosion is defined as irreversible loss of dental hard tissue by a chemical process that does not involve bacteria. Dissolution of mineralized tooth structure occurs upon contact with acids that are introduced into the oral cavity from intrinsic (e.g. gastroesophageal reflux, vomiting) or extrinsic sources (e.g. acidic beverages, citrus fruits). This form of tooth surface loss is part of a larger picture of toothwear, which also consists of attrition, abrasion, and possibly, abfraction. Table 13-2 lists the definitions of each of these forms of tooth surface loss or tooth wear.
Erosion of tooth substance is mainly due to contact with acidic media either by way of foodstuff or by iatrogenic exposure. There could be either extrinsic or intrinsic sources of acid that could cause this mode of tooth substance loss. Examples of extrinsic acids (source outside the body) are acidic beverages, foods, medications or environmental acids. The most common of these are dietary acids. It can be seen that most fruits and fruit juices have a very low pH (high acidity). Carbonated drinks and sports drinks are also very acidic. Several studies have found that the frequency of consumption of acidic drinks was significantly higher in patients with erosion than without. This finding is of concern, particularly since children and adolescents are the primary consumers of these drinks. With consumption of acidic drinks identified as a risk factor in erosion, this amount of soft drink consumption will likely lead to an increase in prevalence of erosion. The erosive potential of beverages does not depend on pH alone. Other components of beverages, such as calcium, phosphates, and fluoride may lessen erosive potential. Also, factors such as frequency and method of intake of acidic beverages as well as the toothbrushing frequency after intake may influence susceptibility to erosion.
Therefore, the role(s) of confounders like oral hygiene status, complicate the role of acids per se which necessitates further investigation to clarify the relationship between acidic beverage intake and dental erosion.
Medications that are acidic in nature can also cause erosion via direct contact with the teeth when the medication is chewed or held in the mouth prior to swallowing. Numerous case reports exist describing extensive erosion secondary to chewing vitamin C preparations or hydrochloric acid supplements. Less common sources of extrinsic erosive acids are related to occupational and recreational exposure. Chromic, hydrochloric, sulfuric and nitric acids have been identified as erosion-causing acid vapors. They are released into the work environment during industrial electrolytic processes. However current work safety standards make this type of erosion very rare. Dental erosion has been reported in swimmers who work out regularly in pools with excessive acidity as well as individuals who are occupational wine-tasters.
Intrinsic causes (acid source inside the body), for erosion are gastric acids regurgitated into the esophagus and mouth. Gastric acids, with pH levels that can be less than 1, reach the oral cavity and come in contact with the teeth in conditions such as gastroesophageal reflux and excessive vomiting related to eating disorders. The association of gastroesophageal reflux disease (GERD) with dental erosion has been established in a number of studies in adults (Figs. 13-6, 13-7). GERD is a common condition, estimated to affect 7% of the adult population on a daily basis and 36% at least one time a month. In this condition gastric contents pass involuntarily into the esophagus and can escape up into the mouth. This is caused by increased abdominal pressure, inappropriate relaxation of the lower esophageal sphincter or increased acid production by the stomach. However, GERD can also be ‘silent’ with the patient unaware of his or her condition until dental changes elicit assessment for the condition.
Figure 13-6 Gastroesophageal reflux disease (GERD) was discovered in this 19-year-old boy who exhibited early generalized erosion (arrow A).
Note the preservation of the enamel at the gingival crevice (arrow B).
Chronic, excessive vomiting has long been recognized as causing erosion of the teeth. The patient with an eating disorder such as anorexia nervosa or bulimia is the classic example. The problem was first reported by Hellstrom and Hurst in 1977. Many reports and reviews have been published on the topic since that time. Although erosion caused by vomiting typically affects the palatal surfaces of the maxillary teeth, it is also common for individuals with eating disorders to consume large amounts of acidic beverages and fresh fruits (Tables 13-3, 13-4). This results in another source of acid exposure, primarily affecting the labial surfaces of the teeth. In addition, treatment for bulimia may include use of antidepressants or other psychoactive medications that may cause salivary hypofunction. Therefore, the cause of erosion cannot be reliably determined from its location.
Erosion associated with alcoholism is caused by frequent vomiting. Other causes of vomiting that may cause erosion include gastrointestinal disorders such as peptic ulcers or gastritis, pregnancy, drug side effects, diabetes or nervous system disorders.
The fluctuations in pH of saliva is mainly kept in balance by the buffering capacity of saliva. This property is largely due to the bicarbonate content of the saliva which is in turn dependent on the salivary flow rate. Bicarbonate concentration also regulates salivary pH. Therefore, there is a relationship between salivary pH, buffering capacity and flow rate, with pH and buffer capacity increasing as flow rate increases. Normally, when an acid enters the mouth, whether from an intrinsic or extrinsic source, salivary flow rate increases, along with pH and buffer capacity. Within minutes, the acid is neutralized and cleared from the oral cavity and the pH returns to normal. Patients with erosion were found to have lower salivary buffer capacity when compared with controls in several studies. In other studies, low whole salivary flow rates in patients with erosion were determined to be the major difference. Therefore, salivary function is an important factor in the etiology of erosion. Since many common medications and diseases can lower salivary flow rate (xerostomia), both whole and stimulated, it is important to assess salivary characteristics when evaluating a patient with erosion.
Identification of the etiology is important as a first step in management of erosion. If excessive dietary intake of acidic foods or beverages is discovered, patient education and counseling are important. If the patient has symptoms of GERD, then he/she should be referred to a medical doctor for complete evaluation and institution of therapy if indicated. A patient with salivary hypofunction may benefit with the use of sugarless chewing gum or mints to increase residual salivary flow. The use of oral pilocarpine (Salagen) may be beneficial in patients with dry mouth caused by Sjögren’s syndrome or post-therapeutic head and neck radiation. A patient suspected of an eating disorder should be referred to a medical doctor for evaluation.
In some cases, an etiologic agent is not identifiable. In other cases, the etiologic agent may be difficult to control, such as the problem of alcoholism. However, regardless of the cause, it is important to follow preventive measures to prevent the progress of erosion. There are several preventive measures that can be taken to control tooth erosion. These are listed in Table 13-5. Patient education is of paramount importance. Much of erosion prevention depends on the compliance of the patient with dietary modification, use of topical fluorides, use of occlusal splint, etc.
Abfraction is currently described as a mode of tooth loss which has clinical and circumstantial evidence. Till recently this type of tooth loss which is mainly confined to the gingival third of the clinical crown was thought to be the result of toothbrush abrasion. It is proposed that with each bite, occlusal forces cause the teeth to flex though little. Constant flexing causes enamel to break from the crown, usually on the buccal surface. The physiological basis of this type of tooth substance loss held that, while not providing a complete explanation, does offer a significant clue to the real cause of this troubling phenomenon. Grippo, in 1991, coined the term abfraction to describe the pathologic loss of both enamel and dentin caused by biomechanical loading forces (Fig. 13-8). He stated that the forces could be static, such as those produced by swallowing and clenching; or cyclic, as in those generated during chewing action. The abfractive lesions were caused by flexure and ultimate material fatigue of susceptible teeth at locations away from the point of loading. The breakdown was dependent on the magnitude, duration, direction, frequency, and location of the forces.
Sclerosis of primary dentin is a regressive alteration in tooth substance that is characterized by calcification of the dentinal tubules. It occurs not only as a result of injury to the dentin by caries or abrasion but also as a manifestation of the normal aging process. For many years it has been known that if a ground section of a tooth with a very shallow carious lesion of the dentin is examined by transmitted light, a translucent zone can be seen in the dentin underlying the cavity (Fig. 13-9). This was readily recognized as being due to a difference between the refractive indices of the sclerotic or calcified dentinal tubules and the adjacent normal tubules. Both Beust and Fish showed that dyes do not penetrate those dentinal tubules that are sclerotic as a result either of age or of a slowly progressive type of dental caries.
The exact mechanism of dentinal sclerosis or the deposition of calcium salts in the tubules is not understood, although the most likely source of the calcium salts is the fluid or ‘dental lymph’ within the tubules. The increased mineralization of the tooth decreases the conductivity of the odontoblastic processes. In addition, the sclerosis slows an advancing carious process.
Sclerotic dentin under a carious lesion was shown by Hodge and McKay to be actually harder than adjacent normal dentin. Subsequently, Van Huysen, Hodge, and Warren confirmed the fact that sclerotic dentin is more highly calcified than normal dentin by employing a unique adaptation of the X-ray absorption technique in which ground slabs of teeth were photographed by X-rays and the degree of radiopacity in areas of normal and sclerotic dentin was measured.
‘Dead tracts’ in dentin are seen in ground sections of teeth and are manifested as a black zone by transmitted light but as a white zone by reflected light (Fig. 13-9). This optical phenomenon is due to differences in the refractive indices of the affected tubules and normal tubules. The nature of the change in the affected tubules is not known, although these tubules are not calcified and are permeable to the penetration of dyes.