Damion Francis TMRI-ERU Dental Caries Damion Francis TMRI-ERU

Eruption Mechanisms of tooth eruption are complex Teeth eventually appear in mouth through a combination of growth of supporting bone Elongation of tooth root and growth of pulp

Nutrition and Teeth Prenatal nutrition and developing teeth Prenatal nutrition has very little effect on the developing tooth Primary teeth begin to calcify in utero Relatively protected from lack of calcium Mother provides calcium needed during pregnancy Ingestion of tetracyclines and high flouride levels by mother causes discoloration in utero

Postnatal nutrition and developing teeth Adequate calcium in a balanced diet is important to tooth development 1950’s vit D was postulated to be important to enamel quality but evidence are lacking to support this in modern research Osteoporosis as no effect on teeth

Nutrition and Dental Caries Direct cause-and-effect relationship between nutritional status and dental caries Malnutrition is associated with retarded exfoliation of primary teeth However unclear if cause by the process itself or the longer time before exfoliation Permanent teeth eruption seem to be unaffected but have higher rates of caries

Enamel Integrity Tooth enamel structure may be damaged by trauma or acid demineralization Loss of the tooth mineral structure begins when enamel surface pH is below 5.7 to 5.5 Normal Neutral pH of the oral cavity is around 6

Dynamic process of demineralization and remineralization is guided by several factors: Oral bacteria, salivary flow and composition, presence of fluoride, tooth integrity and dietary habits Equilibrium shifting of these factors towards demineralization results in enamel dissolution and hence caries formation Calcium and phosphate ( pH) as well as fluoride, can help remineralize affected areas if the process has not reached the cementoenamel junction

Tooth integrity exists when these processes occur without net loss of tooth mass Carious lesions results when the rate of demineralization exceeds the rate of remineralization over an extended time

Diet and Enamel Decalcification Dental erosion is the loss of dental hard tissues (typically the enamel) caused by local effect of acid on the teeth Acid may come from sources such as citrus fruits, acidogenic sport drinks, snacks, carbonated beverages etc. Excessive acidic food or beverages over time may cause enamel dissolution

Further facilitated by xerostomia xerostomia as the natural protection by saliva is absent Important to differentiate this type of erosion from the caries process Acid produced from plaque bacteria causes the enamel demineralization

Caries Process Dental caries is a multifactorial disease Involves demineralization of the enamel and dentin Bacteria in dental plaque metabolize fermentable carbohydrates into organic acids Below the critical pH proteolytic enzymes break down the organic component

Caries Individual Susceptibility

The length of exposure is influenced by a food’s inherent retention in the mouth Eg. Liquids are cleared from the mouth more rapidly than solids; and foods that stimulate salivary flow though their consistency or chemical composition are cleared more rapidly than bland foods. Proteins from saliva adsorb to the cleaned tooth and form the acquired enamel pellicle

Proteinacious coating allows certain bacteria to start to colonize the tooth protein interactions between bacterial cell wall and pellicle Mature and thickened plaque contains many species of oral bacteria in extracellular matrix material More than 500 species of bacteria present in mouth

Small proportion of these are acidogenic bacteria that use dietary sugars as an energy source They produce acids and are associated with the caries development (not all acidogenic bacteria are cariogenic) In humans the two species of interest are Streptococcus mutans and Streptococcus sobrinus

S. mutans is the major pathogenic bacterial species involved in the caries process Studies show that 93% of children with detectable caries were positive for S. mutans The physiologic characteristics of the S. mutans that make them prime etiological agent in caries include their ability to:

S. mutans Adhere to tooth surface Produce abundant insoluble extracellular polysaccharides from sucrose Rapidly produce lactic acid from a number of sugar substrates Be tolerant to acid Produce intracellular polysaccharide stores

Cariogenic bacteria metabolize sugars to produce energy required for their growth and reproduction The energy source may be exogenous or endogenous Metabolism of mono or di saccharides Once within the cell, glucose enters the Embden-Meyerhof glycolitic pathway

End result is production of Lactic acid and or other organic acids Presence of these acids in dental plaque fluid lowers its optimal pH The interface between tooth and plaque is no longer saturated with calcium and phosphate ions Demineralization starts taking place which may go beyond the dentinoenamel junction

Stephan Curve after 10% sucrose rinse and 24-h-old dental plaque

Acid decalcification progress Bacterial invasion of organic matrix Degradation by the process of proteolysis Carious lesions can occur where plaque can sufficiently colonize such as: Pit and fissure caries (found mainly on the occlusal surfaces of posterior teeth, and in lingual pits of maxillary incisors)

Secondary or recurrent caries Smooth surface caries Arise on intact enamel surfaces other than pit fissure Can be divided into smooth surface caries (i.e., caries affecting the buccal and lingual tooth surfaces) Approximal caries, affecting the contact area of adjoining tooth surface Root surface caries Secondary or recurrent caries

Earliest clinically detectable stage of caries in the enamel is the incipient lesion Characterized by an opaque, white appearance At this stage the process is amenable to remineralization Further mineral loss result in enamel degradation and frank cavitation Only treatment option in most cases is the placement of restoration