DEFINITION OF CARIES: Dental caries is defined asan“irreversible disease of calcifiedtissues of teeth, characterized by demineralization of the inorganicportion and destruction of the organicsubstance of the tooth, which often leadsto cavitation”.
ETIOLOGY Many theories have been proposed but only 3 have stood the test of time 1. Miller’s Chemico – parasitic theory 2. Proteolytic theory 3. Proteolysis - chelation theory
I. CHEMICO PARASITIC THEORY W.D.Miller stated in 1887 that “Dental decay is a chemico - parasitic process consisting of two stages : 1. The decalcification of enamel, which results in its total destruction and 2.The decalcification of dentin as a preliminary stage followed by dissolution of the softened residue .
The acid which caused the decay was derived from fermentation of starches and sugars lodged in the retaining centers on teeth. In his experiment he incubated a mixture of bread, meat and sugar with saliva at body temperature It produced enough lactic acid within 48 hours to decalcify sound dentin
In his hypothesis, Miller assigned essential roles to 3 factors – 1. Carbohydrate substrate 2. Acid which caused dissolution of tooth minerals 3. Oral micro organisms which produce acid and also cause proteolysis.
OBJECTIONS TO THE HYPOTHESIS: -1. Unable to explain predilection of specific sites on tooth to caries.2. Initiation of smooth surface caries not explained.3. Unable to explain why some populations are caries free and some are caries prone.
1. ROLE OF CARBOHYDRATES: - Numerous studies confirm the fact that presence of readily fermentable carbohydrates are responsible for increased caries incidence. Cariogenic carbohydrates are dietary in origin since human saliva contains negligible amounts of carbohydrates.
Cariogenicity of carbohydrates depend upon – frequency of its ingestion, physical form, chemical composition, route of administration and presence of other food components. Thus, carbohydrates in detergent foods are less cariogenic than those in sticky, retentive foods. Polysaccharides are less easily fermented than monosaccharides by the plaque organisms. Meals high in fats, proteins or salt reduce the retentiveness of carbohydrates.
2. ROLE OF MICROORGANISMS: - Two gram positive coccal forms of bacteria have been implicated in dental caries from over a century – L.acidophilus and S.mutans. However, it is now recognized that one or more different types of bacteria are involved in “initiation” of caries and a completely different species of bacteria may be involved in “progression” of caries. Also, a different diet – bacterial interaction is involved in producing root and coronal caries.
The various cariogenic species of bacteria include – S.mutans, S.salivarius, S.sanguis, S.mitior, S.millieri, L.acidophilus, Peptostreptococcus intermedius, A.naeslundi, A.viscosus etc. Different bacteria show selectivity for the tooth surfaces they localize and attack, e.g. S.mutans, Lactobacilli species attack the pit and fissures, while A.naeslundi and A.viscosus prefer root surfaces. The Lactobacilli species and A.naeslundi also show preference to deep dentinal lesions.
3. ROLE OF ACIDS: - It is understood that acids are produced by enzymatic breakdown of sugars by cariogenic bacteria. Acids produced are – Lactic acid mainly and butyric acid to some extent.
4. ROLE OF DENTAL PLAQUE: - Plaque defined as a soft, unmineralized, bacterial deposit or biofilm which forms on teeth and dental prostheses that are not adequately cleaned. Resists cleansing by physiological oral forces like salivary washing and tongue movements but is removable by tooth brushing.
COMPOSITION OF DENTAL PLAQUE => Water – 80% Solids – 20% Dry weight of plaque composed of Bacterial & Salivary proteins – 50% Carbohydrates & Lipids - 25% Inorganic ions, mainly Ca++ & Po4--- - 10%CLASSIFICATION OF DENTAL PLAQUE => Plaque classified as – SUPRAGINGIVAL & SUBGINGIVAL. Supragingival plaque – essential role in causing caries, while subgingival plaque – role in periodontal diseases.
MECHANISM OF FORMATION => Plaque formation proceeds through following stages1. Deposition of a cell free layer, ACQUIRED PELLICLE which is derived from salivary glycoproteins. This layer acts as nutrient for plaque bacteria.
2. Colonization of pellicle by Gram positive bacteria like S.sanguis and S.mutans within 24 hours.3. Maturation of plaque by further colonization with filamentous and other bacteria. Also there is build up of plaque substance by polysaccharides produced by plaque bacteria.
II. PROTEOLYTIC THEORY In contrast to acidogenic theory, this theory postulated by Gottleib, Diamond and Applebaum states that caries is essentially a proteolytic process. According to them, the organic or protein elements like enamel lamellae, rod sheath etc are the initial pathway of invasion by microorganisms.
OBJECTIONS TO THE THEORY: - Out of 0.56% of organic matrix, 0.18% is Keratin. However, no enzyme systems capable of attacking keratins have been isolated so far. Studies in germ free rats have shown that caries can occur in the absence of proteolytic organisms.
III. PROTEOLYSIS – CHELATION THEORYSchatz et al in 1955 proposed that caries occurred as a result of simultaneous degradation of organic substances (Proteolysis) and dissolution of tooth minerals by a process called Chelation.
Chelation is a process of complexing of a metallic ion to a complex substance through a co-ordinate covalent bond resulting in a highly stable, poorly dissociated ionized compound. Examples are – Chlorophyll molecule in green plants where 4 pyrrole nuclei are linked to magnesium and Hemoglobin where 4 pyrrole nuclei are linked to iron.
According to this theory, the initial attack on the tooth is on the organic components of enamel. Breakdown products of the proteolysis have chelating properties which form chelates with mineralized components of enamel and thereby decalcify the enamel even in neutral or even alkaline pH.
OBJECTIONS TO THIS THEORY: - Direct evidence for proteolysis – chelation as a mechanism for causing caries is lacking. Recent studies have shown that saliva as well as plaque do not contain substances in sufficient concentrations to chelate calcium from enamel.
MULTIFACTORIAL CONCEPT OF CARIES ETIOLOGY Dental caries – a multifactorial disease – interplay of 3 primary factors plus time also. Mere presence of bacteria and a suitable substrate on a tooth surface at a given time is not enough to cause caries. So, variations in caries incidence occur because of number of indirect or CONTRIBUTING FACTORS.
CONTRIBUTING FACTORS - TOOTH1. COMPOSITION OF TOOTH: - Structure & composition of a tooth determines initiation and rate of progression of caries. Surface enamel more mineralized than subsurface enamel and is more resistant to caries. It also accumulates more fluoride, zinc, lead ions than subsurface enamel. Therefore in initial carious lesions, the subsurface enamel shows marked demineralization even though the outer enamel is relatively intact.
2. MORPHOLOGIC CHARACTERISTICS: - Deep, narrow occlusal fissures or buccal and lingual pits predispose to caries as they tend to trap food and bacteria. Also enamel is quite thin at the base of such deep pits and fissures. Certain surfaces of teeth are more prone to decay like e.g. in mandibular 1st molars the likelihood of caries in descending order is occlusal, buccal, mesial, lingual and distal. The most susceptible teeth are mandibular 1st molars followed by maxillary 1st , mandibular and maxillary 2nd molars.
3. POSITION: - Malaligned, rotated or otherwise abnormally situated teeth can be difficult to cleanse and are likely to trap food debris and bacteria. This, in susceptible persons is sufficient to cause dental caries.
CONTRIBUTING FACTORS - SALIVA1. COMPOSITION: - Many inorganic and organic components of saliva have been investigated for anti cariogenic effects. In normal circumstances, saliva is supersaturated with calcium and phosphate ions With respect to enamel hydroxyapatite. This not only prevents enamel from dissolving but even tends to precipitate apatite in the surface enamel of carious lesions.
2. pH OF SALIVA: - The “critical” pH at which the inorganic material of tooth begins to dissolve is about 5.5, since above this pH, saliva is supersaturated with Ca and Po4 ions. Although much has been discussed about buffering capacity of saliva, its relation with caries incidence is not so simple! Acid production during caries occurs at a localized site on tooth, which in initial stages at least, is covered by dental plaque. This plaque prevents a free exchange of ions.
3. QUANTITY OF SALIVA: - Caries incidence is significantly higher in people with less or no saliva flow, as is seen in cases of salivary gland aplasia and xerostomia. Continuous flow of saliva is required for mechanical removal of bacteria and food debris from the tooth surfaces.
4. VISCOSITY OF SALIVA: - Viscous saliva is associated with high caries incidence as some studies have reported. The reverse has also been shown to be true in some other studies.
5. ANTIBACTERIAL PROPERTIES: - Saliva contains many antibacterial factors like lysozyme, lactoferrin, sialoperoxidase, bistatin, thiocyanate ion, IgA etc. However their efficacy has been doubtful as saliva always appears to contain bacteria capable of causing caries if carbohydrates are present.
CONTRIBUTING FACTORS - DIET1.PHYSICAL FORM: - Very important factor responsible for difference between caries incidence of primitive and modern man. Already explained that diet of primitive man contained plenty of roughage which mechanically cleansed the teeth of any adhering to the teeth.
Also, the coarse nature of the diet induced early attrition of occlusal and proximal surfaces leading to reduction in food entrapment. Diet of modern man in contrast is soft and lacking in roughage. As a result, food sticks tenaciously to teeth and is not cleansed mechanically.
2. CARBOHYDRATE CONTENT OF DIET: - 0ne of the most important factors in caries process. Observed that different ethnic populations have differing caries incidences – postulated that it could be due to difference in diet, especially carbohydrate content.
Diet of caries free ethnic races contain low amounts of carbohydrates, that too found in fruits and vegetables, while diet of caries prone westerners contains more carbohydrates due to intake of processed food. Exceptions – certain populations in India have a high carbohydrate content yet are relatively caries free.
3. LIPID CONTENT OF DIET: - Medium chain fatty acids and their salts have antibacterial effects at low pH. Mechanism of action not understood. Its potential as anticariogenic food needs more investigation.
4. VITAMIN CONTENT OF DIET: - Of all vitamins, only Vit D and Vit K appear to have some role in the caries process. Vit D may have an indirect effect on caries process. Its deficiency can cause enamel hypoplasia which can make the tooth more susceptible to caries. Vit K has enzyme inhibiting action in carbohydrate degradation cycle. Can be utilized as an anticariogenic agent.
5. CALCIUM & PHOSHORUS CONTENT:- There is no relation between dietary calcium and phosphorus and dental caries.6. FLUORINE CONTENT: - While topical and water fluoridation has been known to be effective in caries control, dietary fluorine may have no role as it is unavailable metabolically.
CONTRIBUTING FACTORS – SYSTEMIC FACTORS1. HEREDITY: - Racial tendency for high or low caries may be explained by heredity. However, local factors like change in dietary habits can change this tendency. Possible that caries tendency may be inherited through tooth form & structure.
2. PREGNANCY & LACTATION: - Commonly observed that during pregnancy, women tend to neglect their oral health owing to all her attention being diverted to that of care for the newborn. Thus increased caries incidence during pregnancy & lactation is more a problem of neglect .
REFERENCES: TEXT BOOK OF ORAL PATHOLOGY : SHAFERS CONSERVATIVE AND OPERATIVE DENTISTRY : STURDEVANTS
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