Dental caries and periodontal diseases are probably the most common chronic dental diseases in the world.
DEFINITION (DENTAL CARIES) Dental caries is a multifactorial microbial infectious diseasecharacterized by demineralization ofthe inorganic and destruction of the organic substance of the tooth.
ETIOLOGY OF CARIES-No universally accepted opinion of etiology of dental caries. 3 theories have evolved: (1) Acidogenic theory (Miller’s chemico- parasitic theory) (2) Proteolytic theory (3) Proteolysis-chelation theory
(1) Acidogenic theory (Miller’s chemico-parasitic theory) : , W.D. Miller stated that, “Dental decay is a chemico-parasitic process consisting of two stages, the decalcification of enamel, which results in its total destruction and decalcification of dentin, as a preliminary stage followed by dissolution of the softened residue. The acid which affects the primary decalcification is derived from the fermentation of starches and sugar lodged in the retaining centres of the teeth.”
ROLE OF CARBOHYDRATES : The cariogenicity of dietery carbohydrate varies with – (1) Frequency of ingestion : > frequency - >caries (2) Physical form :> Sticky, solid carbohydrates - > caries, >Liquid carbohyrates - < caries. (3) Other food constituents : Meals > infats, proteins or salts, < oral retentiveness of carbohydrates.
ROLE OF MICRO-ORGANISMS ANDDENTAL PLAQUE : Bacteriological studies have helped toclarify the role of micro-organisms in theetiology of dental caries. Most commonlyLactobacillus, Streptococcus mutans, andActinomyces species are associated withdental caries. Certain micro-organisms –Initiation of caries Certain micro-organisms– Influence progression of caries. Micro-organisms are located in the complex biofilmoverlying the tooth surface termed as dentalplaque.
ROLE OF ACIDS :The enzymatic breakdown of carbohydrates (sugar), results in the formation of acids, chiefly lactic acid.Localization of acids in dental plaque serves a major role in dental caries.Carbohydrates+Enzymes----Acids(lactic acid)
(2) The Proteolytic theory :Another theory was proposed which claims that the organic portion of the tooth is attacked first with lytic enzymes. This leaves the inorganic portion without amatrix support causing it to be washed away creating cavities.
( 3) The Proteolysis-Chelation theory (Schatz’s theory): This theory states that the bacterial attack on the enamel, initiated by keratinolytic microorganisms, results in breakdown of protein and other organic components of enamel, chiefly keratin. This results in the formation of substances which may formsoluble chelates with mineralized component of tooth and thereby decalcify enamel at a neutral or even alkaline pH. This theory states that initial attack of dental caries is on organic and inorganic portion of enamel simultaneously.
Each of these theories fails to explain allramifications of the disease, but all three agree on the following : For dental caries there must be : (1) Host (2) Flora (3) Substrate
(1) Host – It encompasses : Tooth(composition, location,morphological characteristics), Age, Muscular activity, Habits, Group susceptibility and Environment.
(2) Flora Consists of micro-organisms which are brought in the contact of the tooth via plaque. Micro-organisms mainly associated are – (1)Streptococci (S.mutans, S.salivarius, S.mitis, S.sanguis, S.so brinus)(2) Lactobacilli (L. acidophillus)- secondary invaders (3) Actinomyces, Veillonella
(3) Substrate (Diet) :Third factor in initiation and progression of caries. Physical and chemical characteristics ofdiet determine the relative caries activity.(a) Physical characteristics – Solid, fibrous food, then <caries. (b)Chemical characteristics –Monosaccharides and dissaccharides more detrimental then polysaccharides. Sucrose – most detrimental followed by fructose, lactose, galactose and glucose. >Fluoride - <caries. >Calcium and phosphate - <caries. > Vitamins(A, Bcomplex, C, D) <caries.
SALIVA :Primary means to exert control over the oral flora. Normal oral flora – beneficial to the host. Functions of saliva which maintain normal oral flora and tooth surface integrity – *Bacterial clearance * Direct antibacterial activity *Buffering capacity * Remineralization
DR G.V.BLACK’S CLASSIFICATION FOR DENTAL CARIES
CLINICAL CLASSIFICATION OF DENTAL CARIES : (A) According to the location on individual tooth : (1) Pit and fissure caries (2) Smooth surface caries (3) Root caries/Senile caries
PITS AND FISSURE CARIES,SMOOTH SURFACE CARIES,ROOT SURFACE CARIES
C) According to whether the lesion is anew one attacking a previously intact surface or whether it is occuring around the margins of a restoration : (1) Primary caries (2) Secondary/Recurrent caries
PATHOPHYSIOLOGY OF CARIES :Micro organisms mainly S. mutans and lactobacilli in plaque ! Sucrose or other substrate ! Acid production, mainly lactic acid !Acid from plaque overcomes buffering capacity of salivary bicarbonate ! pH is lowered !
When pH<5.5-critical pH and remains at tooth surface for 20-50 minutes ! tooth mineral acts as buffer and loses Ca and phosphate ions into plaque !this buffering capacity maintains local pH 5.0 ! At pH 5.0, surface remains intact, subsurface mineral is lost Initial carious lesion (incipient caries) !
Incipient lesion may be reversed by remineralization !When subsurface demineralization becomes extensive ! tooth surface collapses ! Cavities (Caries)
DIAGNOSIS OF CARIES : (1) Patient history (2) Visual examination (3) Explorers (4) Radiographs (5) Dental floss/tape (6) Separation of teeth (7) Ammoniated silver nitrate (8) Caries detecting solutions/dyes(9) Digital fiber-optic transillumination
(10) White light endoscopy(11) Endoscopically filtered fluorescence(12) Electroconductivity measurements(13) Quantitative laser fluorescence(14) Direct digital radiology –digitalradiographs, xeroradiography(15) Caries detection using laserfluorescence (diagnodent)(16) Optical coherence tomography(17) CO2 laser(18) Magnetic Resonance Microimaging(MRM)
PREVENTION OF DENTAL CARIES (METHODS) :(1) Increasing the resistance of tooth structure to demineralization (2) Modification of diet (3) Plaque control
(1) Increasing resistance of tooth structure to demineralization : (a) Fluoride exposure – Systemic fluorides: Public water fluoridation (1 ppm), fluoride tablets(1mg NaF or MgF), fluoridated table salt (90mg F/kg or 200 mg NaF/kg and fluoridated milk
(b) Use of pits and fissure sealants c) Remineralization
(2) Prevention of caries by modification of diet : (a) Limitation of sucrose consumption to mealtimes (b) Replacement of sucrose by other sweeteners in foods (Sweeteners like sorbitol, lycasin, xylitol) c) Addition of caries-inhibiting agents tofoods (Fluoride, calcium, phosphates, vitamin K, fatty acids etc.)
(3) Prevention of caries by plaque control : (1) Mechanical method (toothbrushing, flossing) (2) Chemical methods (antibiotics, chlorhexidine and other antiseptics(quaternary ammonium compounds, vitamin c), fluorides) (3) Immunological method (oral, systemic, activegingivosalivary, passive dental immunization)
CHEMICAL PLAQUE CONTROL (CHLORHEXIDINE MOUTHWASH)
TREATMENT : (1) NORMAL LESIONS : No treatment required 1 year clinical examination (2) HYPOCALCIFIED ENAMEL (DEVELOPMENTAL WHITE SPOTS):Treatment is elective, for esthetics, restore defects 1 year clinical examination
(3) INCIPIENT ENAMEL LESIONS : Bitewing radiographs indicated (demineralized white spots)Seal defective pits and fissures as indicated 3 months evaluation – oral flora, MScount, progression of white spots, presence of cavitations
(4) POSSIBLE CAVITATED LESIONS (ACTIVE CARIES ) Bitewing radiographs indicated Restorative treatment indicated3 months evaluation as incipient lesions and pulpal response (5) ARRESTED CARIES No active new cavitationsTreatment is elective, for esthetics, restore defects 1-year clinical examination