1. ETIOLOGY
1.1. Miller’s Chemico – parasitic theory
1.1.1. consisting of two stages
1.1.1.1. 1-decalcification of enamel, which results in its total destruction and the decalcification of dentin as a preliminary stage
1.1.1.2. 2-dissolution of the softened residue
1.1.2. Carbs lodged on teeth Cause Fermentation which lead to Acid => Caries.
1.1.3. Factors
1.1.3.1. Carbohydrate substrate
1.1.3.2. Acid which caused dissolution of tooth minerals
1.1.3.3. Oral micro organisms which produce acid and also cause proteolysis
1.1.4. Objections/issues
1.1.4.1. Unable to explain why caries occurs on specific areas only on teeth.
1.1.4.2. How smooth surface caries begins is not explained.
1.1.4.3. Unable to explain why some populations are caries free and some are caries prone.
1.1.4.4. Unable to explain the phenomenon of arrested caries
1.1.5. Role of carb
1.1.5.1. presence of readily fermentable carbohydrates > increased caries incidence.
1.1.5.2. Cariogenicity of carbohydrates depend upon
1.1.5.2.1. Frequency of its ingestion
1.1.5.2.2. Physical form (sticky/fluid, soft/hard)
1.1.5.2.3. Chemical composition
1.1.5.2.4. Route of administration
1.1.5.2.5. Presence of other food components.
1.1.6. Role of microorganisms
1.1.6.1. gram positive cocci have been implicated in dental caries
1.1.6.1.1. L.acidophilus
1.1.6.1.2. S.mutans
1.1.6.2. Microorganisms mechanism
1.1.6.2.1. initiation
1.1.6.2.2. progression
1.1.6.3. Pits & fissures.
1.1.6.3.1. Streptococci & Lactobacilli
1.1.6.4. root surfaces
1.1.6.4.1. Actinomyces
1.1.7. Role of acid
1.1.7.1. Cariogenic bacteria – break down carbs enzymatically – ACIDS (mainly Lactic acid & some amount of butyric acid).
1.1.7.2. Essential for acids to be localized & retained on tooth surfaces => ((CARIES.))
1.1.7.3. Made possible by (DENTAL PLAQUE )
1.1.8. Role of plaque
1.1.8.1. soft, unmineralized, bacterial deposit or biofilm
1.1.8.2. Resists cleansing by physiological oral forces
1.1.8.2.1. salivary washing
1.1.8.2.2. tongue movement.
1.1.8.3. Removable by tooth brushing.
1.1.8.4. factor for at least the ((initiation)) of caries.
1.1.8.5. MECHANISM OF FORMATION
1.1.8.5.1. Deposition of a cell free layer, ACQUIRED PELLICLE
1.1.8.5.2. Colonization of pellicle by Gram positive bacteria
1.1.8.5.3. Maturation of plaque by further colonization with filamentous and other bacteria
1.2. Proteolytic theory
1.2.1. caries is a proteolytic process.
1.2.2. initial pathway of invasion by microorganisms.
1.2.2.1. enamel lamellae, rod sheath
1.2.3. Objection/issues
1.2.3.1. Out of 0.56% of organic matrix, 0.18% is Keratin.
1.2.3.1.1. No enzyme systems capable of attacking keratins
1.2.3.2. caries can occur in the absence of proteolytic organisms.
1.3. Proteolysis - chelation theory
1.3.1. caries occurred as a result of simultaneous degradation of organic substances (Proteolysis) and dissolution of tooth minerals by a process called (Chelation.)
1.3.1.1. Chelation is a process of complexing of a metallic ion to a complex substance through a co-ordinate covalent bond
1.3.2. initial attack on the tooth is on the organic components of enamel.
1.3.3. Objections/issues
1.3.3.1. No direct evidence for proteolysis – chelation as a mechanism for causing caries.
1.3.3.2. saliva as well as plaque do not contain substances in sufficient concentrations to chelate calcium from enamel.
1.3.3.3. chelation may not be actually responsible for initiating caries
1.4. MULTIFACTORIAL CONCEPT OF CARIES ETIOLOGY
1.4.1. Tooth
1.4.1.1. Composition
1.4.1.1.1. Surface enamel more resistance than Subsurface enamel
1.4.1.1.2. In initial caries
1.4.1.2. Morphological characteristic
1.4.1.2.1. More caries in Deep, narrow occlusal fissures / buccal & lingual pits
1.4.1.2.2. mandibular 1st molars
1.4.1.2.3. Most susceptible teeth
1.4.1.3. Position
1.4.1.3.1. (Misalignment)lead to ( rotation) lead to (crowding) lead to (difficult to cleanse) lead to (trap food debris and bacteria) lead to (susceptible persons) Lead to (dental caries)
1.4.2. Saliva
1.4.2.1. Composition
1.4.2.1.1. Prevents enamel from dissolving
1.4.2.1.2. Precipitates hydroxyapatite in the surface enamel of carious lesions.
1.4.2.2. pH
1.4.2.2.1. between 6.2 – 7.4.
1.4.2.2.2. inorganic portion of tooth begins to dissolve if pH < 5.5.
1.4.2.2.3. acid on tooth beneath dental plaque which prevents buffering ions to neutralize the acid.
1.4.2.3. Quantity
1.4.2.3.1. caries incidence lesser in people with less or no saliva flow,
1.4.2.4. Viscosity
1.4.2.4.1. Viscous saliva = increase in Dental caries
1.4.2.5. Antibacterial factors
1.4.2.5.1. lysozyme, lactoferrin, sialoperoxidase, bistatin, thiocyanate ion, sIgA
1.4.3. Diet
1.4.3.1. Physical factors
1.4.3.1.1. Diet of primitive man - plenty of fiber
1.4.3.2. Carb content
1.4.3.2.1. One of the most important factors in caries process.
1.4.3.3. Lipid content
1.4.3.3.1. medium chain fatty acids and their salts have antibacterial effects at low pH.
1.4.3.4. Vit content
1.4.3.4.1. Vit D - indirect effect on caries process
1.4.3.4.2. Vit K has enzyme inhibiting action in carbohydrate degradation cycle
1.4.3.5. Ca.po4 content
1.4.3.5.1. no relation between dietary calcium and phosphorus and dental caries.
1.4.3.6. Fluoride content
1.4.3.6.1. dietary fluorine may have no role as it is unavailable metabolically.
1.4.3.7. Local factors
1.4.4. Systemic condition
1.4.4.1. Hereditary
1.4.4.1.1. caries tendency may be inherited through tooth form & structure.
1.4.4.2. Pregnancy/lactation
1.4.4.2.1. neglect their oral health owing to all her attention being diverted to that of care for the newborn.
1.4.4.2.2. increased caries incidence during pregnancy & lactation is more a problem of neglect
2. DEFINATION
2.1. irreversible disease of calcified tissues of teeth
2.2. demineralization of the inorganic portion
2.3. destruction of the organic substance of the tooth,
2.4. leads to cavitation
3. EPIDEMIOLOGY
3.1. Occurs universally. No human being is immune.
3.2. Directly linked to dietary habits
3.3. Factors
3.3.1. RACE
3.3.1.1. Generally, Chinese, Blacks, Indians have lesser caries incidence than the Caucasian whites.
3.3.2. AGE
3.3.2.1. More in children
3.3.2.2. Incidence lesser in younger and middle age group.
3.3.2.3. Incidence increase by the older age.
3.3.3. GENDER
3.3.3.1. higher in females than males.
3.3.3.2. due to the fact that teeth in females erupt earlier
3.3.4. FAMILIAL
3.3.4.1. heredity involved
4. CLASSIFICATION
4.1. BASED ON MORHOPLOGICAL SITE
4.1.1. Pit and fissure caries
4.1.1.1. Seen on occlusal surface of molars and premolars
4.1.1.2. buccal and lingual surfaces of molars
4.1.1.3. lingual surface of maxillary incisors
4.1.1.4. Deep pits and fissures more caries.
4.1.1.4.1. Due to poor self cleansing properties
4.1.1.5. enamel at the base of such pits and fissures is (thin)
4.1.1.6. Early lesions
4.1.1.6.1. locations appear brown / black
4.1.1.6.2. “catch” a fine explorer point.
4.1.1.7. Lateral spread
4.1.1.7.1. penetration of dentinal tubules at DEJ.
4.1.1.8. large carious lesion may be present inside with only a pinpoint opening seen on the tooth surface (ACUTE CARIES)
4.1.1.9. progress of caries is much slower and pulpal involvement is also much delayed (CHRONIC CARIES)
4.1.2. Smooth surface caries
4.1.2.1. on proximal surfaces of all teeth
4.1.2.2. on gingival 1/3rd of buccal and lingual surfaces.
4.1.2.3. caries is preceded by formation of dental plaque
4.1.2.3.1. unlike pit and fissure caries.
4.1.2.4. Begins just below the contact point
4.1.2.5. appears initially as a faint white opacity
4.1.2.6. early chalky white spot becomes roughened
4.1.3. CERVICAL CARIES
4.1.3.1. buccal, lingual or labial surfaces.
4.1.3.2. Always occurs as an open cavity.
4.1.3.3. on all the teeth as it is directly related to lack of oral hygiene.
4.1.4. ROOT CARIES
4.1.4.1. Soft progressive lesion that is found anywhere on the root surface
4.1.4.2. seen in teeth of older individuals
4.1.4.2.1. showing gingival recession and exposed root
4.1.4.3. Begins on cementum / dentin
4.1.4.4. most frequently on buccal and lingual root surfaces.
4.1.4.5. Dental plaque essential for initiating root caries.
4.1.4.6. after reaching dentin, progression is slower than coronal dentin
4.2. BASED ON RATE OF PROGRESSION
4.2.1. Acute dental caries
4.2.1.1. rapid clinical course and results in early pulpal involvement
4.2.1.2. Small, pin-point entry even though caries spreads rapidly at DEJ => large internal cavitation.
4.2.1.3. Affected dentin - stained light yellow compared to deep brown / black of chronic caries.
4.2.1.4. RAMPANT DENTAL CARIES
4.2.1.4.1. sudden, rapid destruction of teeth affecting even relatively caries free surfaces
4.2.1.4.2. Prominently observed in (deciduous dentition) and (permanent dentition of teenagers(.
4.2.1.5. NURSING BOTTLE CARIES
4.2.1.5.1. baby bottle syndrome and bottle mouth syndrome.
4.2.1.5.2. Due to
4.2.1.5.3. Absence of caries in mandibular teeth distinguishes it from ordinary rampant caries.
4.2.2. Chronic dental caries
4.2.2.1. Progresses slowly - involves pulp much later than acute caries.
4.2.2.2. Adult predilection.
4.2.2.3. ARRESTED CARIES
4.2.2.3.1. caries which becomes static or stationary and does not progress any further.
4.2.2.3.2. both deciduous and permanent dentition.
4.2.2.3.3. on occlusal surface caries.
4.2.2.3.4. large, open cavity in which there is no food retention
4.2.2.3.5. softened decalcified dentin is gradually burnished until it assumes a brown polished appearance.
4.2.2.4. RADIATION CARIES
4.2.2.4.1. patients receiving radiotherapy in head & neck region is called as RADIATION CARIES.
4.2.2.4.2. Xerostomia is a major complication of radiotherapy
4.3. BASED ON WHETHER LESION IS NEW OR UNDER PREVIOUS RESTORATION
4.3.1. Primary (virgin) caries
4.3.2. Secondary (recurrent) caries
4.3.2.1. around or beneath an existing restoration.
4.3.2.2. due to inadequate extension of restoration resulting in food impaction
4.3.2.3. if a restorative material is not properly adapted to margins
5. HISTOPATHOLOGY
5.1. Caries process in enamel progresses through following stages
5.1.1. Early submicroscopic lesion
5.1.2. Phase of nonbacterial enamel crystal destruction
5.1.3. Cavity formation
5.1.4. Bacterial invasion of enamel
5.1.5. Cavity formation+ Bacterial invasion Occur almost simultaneously
5.2. Early lesion - smooth surface
5.2.1. Earliest changes - chalky white spot
5.2.2. EM
5.2.2.1. loss of inter rod enamel
5.2.2.2. Accentuation of striae of Retzius (1) and perikymata
5.2.3. conical shape
5.2.3.1. base towards enamel surface
5.2.3.2. apex towards DEJ
5.2.4. Four zones as seen from deepest advancing zone towards DEJ
5.2.4.1. Translucent zone
5.2.4.1.1. Not seen clinically & radiologically.
5.2.4.1.2. due to formation of submicroscopic pores at:
5.2.4.1.3. slightly more porous than normal enamel
5.2.4.2. Dark zone(positive zone)
5.2.4.2.1. Superficial to translucent zone.
5.2.4.2.2. Pore volume is 2 – 4%.
5.2.4.3. Body of lesion
5.2.4.3.1. The bulk of the lesion
5.2.4.3.2. between relatively unaffected surface zone and dark zone.
5.2.4.3.3. pore volume of 5%
5.2.4.3.4. about 25%
5.2.4.4. Surface zone
5.2.4.4.1. only remains intact
5.2.4.4.2. Pore volume of only 1%.
5.2.4.4.3. this zone is demineralized by the time caries penetrates dentin.
5.3. Early lesion - pit n fissure
5.3.1. not much different from smooth surface.
5.3.2. starts on both side of fissure
5.3.3. visual changes like yellow or brown discoloration
5.3.4. enamel being usually thin at the base of pits and fissures
5.3.5. cone shaped lesion
5.3.5.1. base towards DEJ
5.3.5.2. apex directed occlusally.
5.4. Dentin early changes
5.4.1. beneath enamel before any cavity has formed.
5.4.2. Acids formed in enamel causes diffuse into dentin which leads to demineralize dentin.
5.4.3. Bacteria invade dentin easily.why?
5.4.3.1. due to pathway provided by dentinal tubules (DT).
5.4.4. Bacteria liberate proteolytic enzymes which leads to destruction of organic matrix of dentin
5.4.5. First change
5.4.5.1. fatty degeneration of the tome’s fibers
5.4.5.1.1. Tome’s fibers=odontoplastic process
5.4.6. Followed by dentinal sclerosis
5.4.6.1. minimal in rapidly advancing acute caries and maximum in slow, chronic caries.
5.4.6.2. considered as a protective measure by DT to seal off
5.4.6.3. Behind the zone of dentinal sclerosis a narrow zone of decalcification
5.4.6.4. only a few tubules are invaded even before clinical evidence of caries.
5.4.6.4.1. These bacteria are called “Pioneer bacteria”.
5.5. Dentin advanced changes
5.5.1. Decalcification of DT continues
5.5.1.1. Lead to
5.5.1.1.1. confluence / junction of DT
5.5.2. junction and breakdown of adjacent DT leads to formation of “Miller’s liquefaction foci”.
5.5.3. Dentinal caries zone
5.5.3.1. ZONE 1 – Zone of fatty degeneration of Tomes’ fibers
5.5.3.2. ZONE 2 – Zone of dentinal sclerosis
5.5.3.3. ZONE 3 – Zone of decalcification
5.5.3.4. ZONE 4 – Zone of bacterial invasion
5.5.3.5. ZONE 5 – Zone of decomposed dentin