Dental Caries

2. Dental Caries

3. Definition “CARIES” Latin word meaning “rot” or “decay”. WHO defines as a localised post eruptive, pathological process of external origin, involving softening of hard tooth tissues and proceeding in to formation of cavity.

4. Dental caries is an infectious irreversible microbial disease of the calcified tissues of the teeth, characterized by demineralization of the inorganic portion & destruction of the organic substance of the tooth, which often leads to cavitations. (shafer’s)

5. Classification

10. G.V.BLACK’S CLASSIFICATION Class 1 Class 2 Class 3 Class 1 lesions: Involving pits,fissures and defective grooves. Class 2 lesions: Involving proximal surfaces of the bicuspids and molars. Class 3 lesions: Involving proximal surfaces of anterior teeth that do not involve incisal angle.

11. Class 4 Class 5 Class 6 Class 4 lesions: Lesions found on the proximal surfaces of anterior teeth that involves the incisal angle. Class 5 lesions: Lesions that are found at the gingival third of the facial and lingual surfaces of anterior and posterior teeth. Class 6 (Simon’s modification): Lesions involving cuspal tips and incisal edges of teeth.

12. World Health Organization (WHO) System In this classification the shape and depth of the caries lesion is scored on a four point scale D1. clinically detectable enamel lesions with intact (non cavitated) surfaces D2. Clinically detectable cavities limited to enamel D3. Clinically detectable cavities in dentin D4. Lesions extending into the pulp

13. Pit and Fissure Caries Seen on : -Occlusal surface of molars and premolars -Buccal and lingual surface of molars -Palatal surface of max incisors Pits and Fissures with high steep walls and narrow bases are more prone to caries-poor self cleansing features Appear brown or black, soft and catch a fine explorer tip

14. Enamel bordering it appear bluish white as it is undermined Presence of large carious lesion with tiny point of opening (mistaken idea of “INTERNAL CARIES”-phenomena of tooth getting decayed from inside outward)

15. Smooth Surface Caries Seen on: -proximal surfaces -gingival third of buccal and lingual surfaces Preceded by formation of microbial plaque Proximal caries begins just below the contact point Initially appears as a faint white opacity without loss of enamel continuity-well demarcated Later becomes roughened due to superficial decalcification of enamel

16. Root caries • Katz and his associates, studied the distribution pattern, and found that teeth frequently affected are first mand molars>mand premolars>max cuspids • Proximal surfaces are more affected in max arch and buccal surfaces in mand arch The Prevalence and Intra-oral Distribution of Root Caries in an Adult Population, Caries Res 1982,16:265-272. Hazen defined as “a soft, progressive lesion that is found anywhere on the root surface that has lost connective tissue attachment and is exposed to the oral environment”. Seen in older age groups with significant gingival recession and exposed roots. Previously called as “caries of cementum”.

17. Stamm and Banting, studied effect of fluoride on root caries and found, lifelong consumption of fluoridated water is capable of significantly reducing root caries which is becoming a growing dental public health problem in adult population. J Am Dent Assoc. 1990 Feb;120(2):143-9 Initiates on mineralized cementum and dentin Evidence suggest that microorganisms involved in root caries are different from coronal caries, being filamentous rather than coccal Microorganisms invade cementum along sharpey’s fibers Cementum forms in concentric layers has lamellatedapperance, microorganisms spread laterally in various layers

18. Acute dental caries Rapid clinical course Results in early pulp involvement Two chronological periods commonly affected are 4-8 yrs and 11-18 yrs Initial entrance of lesion remains small-saliva cannot enter the small opening, to neutralize the acid formed

19. Acute dental caries Occurs frequently in children and young adults-dentinal tubules are large and open and show no sclerosis Process is so rapid, little time for reparative dentin deposition seen Dentin is light yellow Pain is an apt feature

20. Rampant caries Sudden, rapid and almost uncontrollable destruction of teeth, affecting the surfaces of teeth that are relatively caries free. Includes-proximal and cervical surfaces of mandibular incisors also. Caries increment of 10 or more new carious lesions over one year.

21. Affects both Primary dentition and Permanent dentition of teenagers. Carious process is so severe that only root stumps are left

22. Nursing bottle caries(nursing caries,baby bottle syndrome,bottle mouth syndrome) Attributed to prolonged use of: -nursing bottle containing milk or milk formula, fruit juice or sweetened water -Sugar or honey-sweetened pacifiers Clinically seen as widespread carious destruction of deciduous teeth

23. Nursing bottle caries(nursing caries,baby bottle syndrome,bottle mouth syndrome) Most commonly 4 max incisors followed by first molars then cuspids Absence of caries in mand incisors distinguishes this from rampant caries

24. Adolescent caries Acute caries attack at 11-18 yrs of age Seen on surfaces relatively considered immune to caries Seen as small opening in enamel with extensive undermining Rapid progression-no time for reparative dentin formation

25. Chronic dental caries Progresses slowly and involves pulp in much later phase Entrance to lesion is much larger Deep brown in color Much destruction of tooth surface Minimum softening of dentin

26. Moderate lateral spread of caries at DEJ Slow progress of lesion-allows sufficient time for :- -sclerosis of dentinal tubules -secondary dentin deposition Pain not common-protection to pulp by secondary dentin

27. Recurrent caries Occurs in the immediate vicinity of a restoration. Usually seen near the gingival margins of class 2 and class 5 restorations and rarely on class1 restorations. Soft at the margin of filling and detected with an explorer

28. Recurrent caries Due to poor adaptation of filling material to the cavity produces “leaky margin”. Besic in 1943 studied the fate of bacteria sealed in dentinal tubules and noted that lactobacilli died out, while streptococci persisted.

29. Arrested caries Caries becoming static or stationary and does not show any tendency for further progression. Both dentitions affected Appears as brown stained, polished and is hard “Eburnation of dentin”- caries on occlusal surfaces characterized by a large open cavity and superficially softened and decalcified dentin is gradually burnished taking up brown color. Sclerosis of dentinal tubules and secondary dentin formation seen

30. Radiation caries • Development of rampant caries in patients undergoing radiation therapy in head and neck region. • Increased viscosity and low pH of saliva seen after irradiation • Del Regato in 1939 observed xerostomia as a complication of radiation therapy and postulated that caries development may be due to modification of saliva secretion • Frank et al (1965)and Baden(1970) explained 3 forms of dental defects as a consequence of irradiation:- • Caries like lesion:-completely encircling the neck of tooth leading to crown amputation • Brown-black discoloration • Spot depression-spreads from incisal or occlusal edges to labial and lingual surfaces.

31. Incipient caries • Seen as a white spot • Contrasts well with more transparent enamel • Caries attack changes the optical behavior of affected enamel-becomes opaque as porous enamel scatters more light than sound enamel • Requires air-drying to become visible • Usually confused with white developmental defects of enamel, so differentiated by:- • Position-usually away from gingival margin • Shape-unrelated to plaque accumulation • Symmetry-usually affect the contralateral tooth • On wetting-carious lesion disappears while developmental defects persists.

32. Occult caries Also known as hidden caries A lesion not clinically diagnosed but detected only on radiographs Acc to Seow in 2000,prevalence range from 0.8% in premolars in 14-15 yrs and 50% in 20 yrs. “Fluoride syndrome or fluoride bombs”-itis believed that increased fluoride exposure encourages remineralization, slowing down caries progression in enamel while cavitation continues in dentin and the lesion becomes masked by a relatively intact enamel surface.

33. EPIDEMIOLOGY Caries in Prehistoric man Caries is considered a disease mainly of modern civilization, as prehistoric humans rarely suffered from it. Caries in such persons was seen to occur below the contact areas & also on the CEJ.

34. Caries in Modern man Occurs universally. No human being is immune. Commonest infection to occur in oral cavity. Directly linked to dietary habits of modern man – processed, soft food. Primitive man’s diet was coarse, raw and mostly uncooked.

35. FACTORS AFFECTING CARIES PREVALENCE RACE: People living in same geographical area but belonging to different race have differing caries incidence. Chinese, Blacks, Indians have lesser caries incidence than the Caucasian whites.

36. AGE: Dental caries more prevalent in children up to 12 years. Incidence decreases somewhat in younger and middle age group. Incidence increases again by the older age.

37. GENDER: Incidence of caries is significantly higher in females than males. This may be due to the fact that teeth in females erupt earlier compared to males.

38. FAMILIAL: Hereditary pattern is evident. Children of parents with low caries experience also show lesser caries incidence and vice versa.

39. ETIOLOGY OF DENTAL CARIES • early theories Worm theory Endogenous theories Chemical theory Parasitic theory • modern theories Acidogenic theory Proteolytic theory Proteolysis chelation theory Sucrose chelation theory Auto-immune theory Sulfatase Theory

40. Early Theories • The Legend of Worms – • Earliest mention is from ancient Sumerian text (5000BC) known as the “Legend of worms”. • Caries is caused by worms which drank blood of the teeth & fed on roots in the jaws.

41. 2. ENDOGENOUS THEORIES Humoral Theory • Greek physicians • Dental caries is produced by internal actions of acids & corroding humors & an imbalance in these humors resulting in disease. • Blood (sanguine) • Phlegm (phlegmatic) • Black bile (melancholic) • Yellow bile (choleric)

42. Vital Theory of tooth decay • Hippocrates, Galen • Proposed that tooth decay originated like a bone gangrene, from within the tooth itself. • Penetration of caries into dentin and pulp without detectable catch on the surface • Hunter, 1778, proposed that caries arose secondary to pulpal inflammation.

43. 3. CHEMICAL THEORY Parmly, 1820s. • He observed that caries affected externally not internally. • He proposed that an unidentified chymal agent was responsible. Robertson, 1835 • Supported Parmly • DC was caused by acid formation by fermentation of food particles around the teeth.

44. 4. PARASITIC THEORY / SEPTIC THEORY Erdl, 1843. • He observed filamentous parasites (parasitischevegetabil) assoc. with carious lesions. Fincus, 1847 • Described filamentous organisms in enamel cuticle & carious lesions. …denticolae

45. Parasitic theory was disseminated by 2 German physicians Leber& Rottenstein 1867 • Caries initiation is by an undefined acid which rendered enamel porous & facilitated the formation of a bed of filamentous microrg. on the enamel surface. Underwood & Miles 1881 • Combined actions of germs & acids • Acc. To them organisms 1st attacked the organic material & feeding upon it created an acid that removed lime salt.

46. Modern Theories 1) MILLER’s CHEMOPARASITIC THEORY / ACIDOGENIC THEORY • Willoughby D Miller 1890 • blend of 2 theories • States that caries is produced by acids produced by microorganisms of the mouth.

47. hypothesis • DC is a chemoparasitic process consisting of 2 stages: * Decalcification of enamel & dentin which leads to total destruction ( preliminary stage). ** Dissolution of the softened residue (subsequent stage). • The acid which affects the primary decalcification is derived from the fermentation of starches & sugars lodged in the retaining centers of the teeth.

48. experiments to prove his theory • Bread & sugar when incubated in vitro with saliva at body temp., there was acid production within 48 hours enough to decalcify sound dentin. • He isolated many microorg from the oral cavity, many of which were acidogenic & some proteolytic. Since many forms produce lactic acid, he believed that caries was not caused by a single organism , but by a variety of them.

49. Evidences • Acid was present within deep carious lesions. • Bread or sugar incubated at 37°C with saliva could decalcify the entire crown of a tooth. • There’s correlation btwn cariogenic bacteria in saliva & caries activity. • Inoculation of acidogenic bacteria in gnotobiotic rats on CHO diet induced caries. • pH of cavities was lower than those of normal teeth

50. Drawbacks • Unable to explain the predilection of specific sites on a tooth to caries. • Initiation of smooth surface caries. • why some populations are caries free • phenomenon of arrested caries.