DENTAL PLAQUE BY DR. MANISHA MISHRA
Dental Plaque • Yellowish white soft, tenacious, amorphous material deposited on tooth surface Formation Adherent layer of mucinous material from saliva Colonisation of layers by diffusion of micro organisms w/n 48 hrs whole layers constitute of microorganisms
Plaque deposition occurs in interproximal surface of posterior teeth i.e,labial and gingivial for lower and labial and palatal for upper teeth. Types: • Supragingival • Infragingival Composition: • 70-90%-Microorganisms • 10-30%-Inorganic and Organic substances
Dental Plaque Heavy staining and calculus deposits exhibited on the lingual surface of the mandibularanterior teeth, along the gumline.
Plaques initially populated by following: Organisms: • Gram positive Cocci/Bacilli • Gram negative Cocci and Bacilli • Fungus—Candida albican,Actinomycosisisraelli
1.Gram positive cocci— • Streptococcus-mutans,viridans,mitis,milleria,salivaris,pyogens,Staph- aureus,albus 2.Gram negative cocci— • NG,NM,NC 3.Gram positive bacilli— • Lactobacillus- acidiphilus,fermentation,odentolyticus 4.Gram negative bacilli— • H.influenzae,B.pertusis,Fusiform bacteria
Other than organisms: • Inorganic—Calcium,Sodium, Potassium,Phosphorus • Organic— Protein,Lipid, desquamated essential FA,Leucocytosis,Cells.
Growth of plaque • Multiplication of existing bacteria • Addition of new bacteria • Accumulation of metabolic products of bacteria • Food debris from diet Plaque leads to: • Acids released from dental plaque lead to demineralization of the adjacent tooth surface, and consequently to dental caries. • Saliva is also unable to penetrate the build-up of plaque and thus cannot act to neutralize the acid produced by the bacteria and remineralize the tooth surface. • They also cause irritation of the gums around the teeth that could lead to gingivitis, periodontal disease and tooth loss. • Plaque build up can also become mineralized and form calculus (tartar).
DENTAL PLAQUE Inadequate removal of plaque caused a build up of calculus (dark yellow color) near the gums on almost all the teeth.
Prevention 1. Mechanical – Brushing , Flossing • Brush your teeth twice daily using a fluoride-based toothpaste. • Floss your teeth daily, or use an interdental cleaner. 2. Chemical – Mouth wash 3. Food intake – • Coarse, Dry (Avoid 3s sweet, sticky, soft) • Eat a balanced diet. • Avoid using tobacco products. • Limit the number of snacks you eat throughout the day. 4.Gingival massage
Dental Calculus (TARTAR) • Hard deposit formed on the tooth (due to mineralisation of dental plaque) • Plaque converted to calculus in 50 – 60 days Classification • Supragingival – coronal to gingival margin • Subgingival – below the crest of gingival margin
Supragingival calculus: • Colour=Yellowish to white ,Blackish • Consistency=clay like • Maximum occurs in Upper buccal region of molar teeth,lingual and interproximal surface of lower to anterior teeth. Subgingival calculus: • Dense brown to greyish black in colour
Composition: • 70-90%=Inorganic material • 10-30%=Organic material • Calculus formation can result in a number of clinical manifestations: • including bad breath • receding gums and • chronically inflamed gingiva.
Prevention • As in Plaque (oral hygiene) Treatment • Scaling 1. Manual and 2. Ultrasonic scaling
Dental caries • Irreversible progressive bacterial damage to the hard structures of the tooth characterised by demineralization resulting in the formation of a cavity Etiology --Decalcification by bacterial acid followed by destruction of all other tooth tissue • No theory is universally accepted • Acidogenic theory • Proteolysis chelation theory • Proteolytic theory
Acidogenic theory Dental caries is a sugar-dependent infectious disease. • Acid is produced from metabolism of carbohydrate by plaque bacteria, which results in a drop in pH at the tooth surface. • In response, calcium and phosphate ions diffuse out of enamel, resulting in demineralization. • This process is reversed when the pH rises again. • Caries is therefore a dynamic process characterized by episodic demineralization and remineralization occurring over time. • If destruction predominates, disintegration of the mineral component will occur, leading to cavitation.
Proteolytic theory • In addition to acid, proteolytic substances produced by plaque bacteria breakdown the organic portion of enamel and dentine
Proteolysis Chelation theory • Bacterial attack on enamel is initiated by keratinolytic bacteria causing breakdown of enamel protein • Organic and inorganic portion of enamel undergoes demineralization by formation of chelates
Saliva and caries • Saliva acts as an intra-oral antacid, due to its alkali pH at high flow-rates and buffering capacity. • In addition saliva: • ⇓ plaque accumulation and aids clearance of foodstuffs. • Acts as a reservoir of calcium, phosphate, and fluoride ions, thereby favouringremineralization. • Has an antibacterial action because of its IgA, lysozyme, lactoferritin, and lactoperoxidasecontent.
CARIOGENIC BACTERIA: • Streptococcus mutans • Streptococcus viridans • S. salivaries • S. mitis • S. sanguis • Lactobacillus
Properties of bacteria • Ability to produce acid by fermentation of sugars • Ability to polymerise sugars into long chain polysaccharides which make • plaque adhere firmly to the tooth surface and • Bacteria to one another • Lactic acid (main) and other is acetic acid
Prerequisites for development of dental caries • Dental plaque containing cariogenic bacteria • Bacterial substrate: sugar • Susceptible tooth surface • If pH < 5 then demineralization occurs
Enamel caries • The initial lesion is visible as a white spot. This appearance is due to demineralization of the prisms in a sub-surface layer, with the surface enamel remaining more mineralized. • With continued acid attack the surface changes from being smooth to rough, and may become stained. • As the lesion progresses, pitting and eventually cavitation occur.
DENTINE CARIES: • Dentine caries comprises demineralization followed by bacterial invasion, • but differs from enamel caries in the production of secondary dentine and the proximity of the pulp.
Diagnosis Early diagnosis is important Good eyesight (and a clean, dry, well-illuminated tooth) • Whitish or blackish spots • Cavity
Investigation • radiographs are useful in the detection of occlusal caries.
Management If lesion confined to enamel , institute preventive measures and keep under review. If lesion has penetrated dentine radiographically, a restoration is indicated unless serial radiographs show that it is static. • Removal of diseased enamel and dentine • Removal of pits and fissures • Restoration by filling • Posterior teeth • Cement & silver amalgam • Anterior teeth • Acid etch technique • RCT –Root canal treatment
Criteria for restoration: • Restoration should be watertight • Form of the tooth should be maintained so that occlusion is normal • Pulp should be protected with insulating cement lining
Prevention • Maintenance of oral hygiene • Proper brushing • Regular scaling • Avoid soft, sticky and sweet diet • Reduce bacterial load • Mouthwash with 0.2% chlorhexidine, betadine • Denial of substrate to plaque bacteria • Use saccharine( an artificial sweetener) as bacteria cannot utilize it • Complete removal of plaque by dentist • Scaling
Fluoride addition • Inhibits demineralization and promotes remineralization of early caries. • Fluoride enhances the degree and speed of remineralization and renders the remineralized enamel more resistant to subsequent attack. • Decreases acid production in plaque by inhibiting glycolysis in cariogenic bacteria. • An ⇑ concentration of fluoride in plaque inhibits the synthesis of extracellular polysaccharide.
Systemic fluoride • Water fluoridation in a concentration of 1 ppm (1 mg F /litre) gives a caries reduction of 50%. • Fluoride tablets • depends upon drinking water content • 1 tab contains 2.2 mg of Na Fluoride • <2 yrs : half tab • 2-12 yrs: 1 tab • > 12 yrs: half tab
Milk with 2.5-7 ppm F has been tried successfully. • Salt is cheap and effective for rural communities in developing countries where water fluoridation is not feasible
Fluorosis (or mottling) occurs due to a long-term excess of fluoride. • It is endemic in areas with a high level of fluoride occurring naturally in the water. • Clinically, it can vary from faint white opacities to severe pitting and discoloration.