2024 Introduction to Dental Caries PDF

INTRODUCTION TO DENTAL CARIES Dr.S.Bredenkamp CLD 100 LEARNING OUTCOMES Provide a definition of dental caries List + explain the theories of dental caries List+ explain the aetiological factors of dental caries List + explain the criteria the classification of caries is based on. List + explain the...

INTRODUCTION TO DENTAL CARIES Dr.S.Bredenkamp CLD 100 LEARNING OUTCOMES Provide a definition of dental caries List + explain the theories of dental caries List+ explain the aetiological factors of dental caries List + explain the criteria the classification of caries is based on. List + explain the Zones of enamel + dentine caries (histopathology) List the differences between infected + affected dentine List + explain how you would detect caries Explain what is meant by caries risk assessment List the criteria for a high caries risk patient List and explain the factors most commonly seen in a high caries risk patient List and explain the factors that help prevent dental caries INTRODUCTION Dental caries is one of the most prevalent chronic disease. It occurs as a result of the interaction between acid producing bacteria + fermentable carbohydrates. The acid present in dental plaque may demineralize enamel + dentine DEFINITION It is a microbial disease of the calcified tissues of the teeth, characterized by demineralization of calcified tissues and destruction of the organic substance of the teeth – Shafer An infectious microbiological disease of teeth that results in localized dissolution and destruction of calcified tissues - Sturdevant A localized post-eruptive pathological process of external origin involving softening of the hard tissue + proceeding to the formation of a cavity - WHO THEORIES Acidogenic Proteolytic Proteolysis-chelation Caries balance concept ACIDOGENIC 1890 Most accepted theory given by Miller It was said that it is a chemico-parasitic process consisting of 2 stages Decalcification of enamel- total destruction as a preliminary stage Dissolution of the softened residue of the enamel + dentine This whole process is supported by the presence of carbohydrates, microorganisms + dental plaque PROTEOLYTIC 1878 Heider Bodecker The organic portion of the tooth plays an important role in the development of dental caries Enamel structures such as the enamel lamellae + enamel rods proves to be the pathways for the advancing microorganisms These invade the enamel lamellae + the acid produced by the bacteria causes damage to the organic content PROTEOLYSIS-CHELATION 1955 Schatz + co workers Enamel is demineralized by chelating agents at neutral pH Bacterial attack on enamel is initiated by keratinolytic microorganisms Breakdown of the protein keratin Formation of soluble chelates which decalcifies enamel at a neutral pH Enamel contains mucopolysaccharides, lipids and citrate which are susceptible to bacterial attack + act as chelators CARIES BALANCE CONCEPT Caries does not result from a single factor Outcome of a complex interaction of pathologic + protective factors Pathological factors are bacteria, poor dietary habits + Xerostomia Protective factors are saliva, antimicrobial agents, fluoride, pit and fissure sealants + effective diet. AETIOLOGY Primary factors Tooth Substrate Bacteria Time period Modifying factors Saliva Primary factors: Tooth Susceptible areas on the tooth involving deep + narrow occlusal fissures, deep buccal or lingual pits, exposed root surfaces Position of the tooth- if a tooth is out of position such as rotated/malaligned – difficult to clean resulting in retention of food + debris hence susceptible. Biochemical structure of teeth – Surface enamel is more mineralized than subsurface enamel. It contains more fluoride than subsurface enamel. Primary factors: Substrate(Diet) Physical nature of diet More refined and less fibrous foods have low clearance from the oral cavity + thus are more responsible for dental caries. Chemical nature of diet Simple carbohydrates like glucose, fructose and sucrose make the diet cariogenic. Complex carbohydrates are not easily fermentable + are thus less cariogenic. Frequency of carbohydrate intake The greater the time lapse between acid attacks better the chances for the repair process (reminerilization) to occur. The lower the frequency of carbohydrate intake the lower the risk of dental caries. Primary factors: Bacteria Streptococcus mutans (SM) main causative factor for caries Ability to adhere to tooth surface, produce abundant amounts of acid + survive + continue metabolism at low pH conditions Ferments the sucrose to produce the extracellular polysaccharide glucan. Glucan assists SM to adhere firmly to the tooth surface + inhibits diffusion of salivary buffers Result- local environment becomes acidic with dissolution of tooth structure. Primary factors: Time The time period which all above three principal factors are acting jointly should be adequate to produce an acidic pH which is critical for the dissolution of enamel -caries Modifying factors: Saliva Composition Calcium + phosphate ions present in the saliva help in remineralization of the very early stages of carious lesion pH The critical pH at which organic material of the tooth begins to dissolve is 5,5. Above this the saliva is saturated with calcium + phosphate ions. Viscosity The higher the viscosity, an increase in the incidence of dental caries Antibacterial Lysozymes, lactoferrin, IgA (antibacterial properties) CLASSIFICATION is based on the following; Anatomical site Lesion is New/Attacking Speed of caries progression Treatment and restoration design Pathway of caries spread Extent of the caries Number of tooth surfaces involved Chronology Tooth surfaces Caries is completely removed/not WHO system Radiographic classification Graham Mount classification Anatomical site Pit and fissure caries- seen in pit and fissures on the occlusal surfaces of posterior teeth + buccal and lingual surfaces of molars + on lingual surfaes of maxillary teeth Smooth surface caries- all smooth surafces Root caries- exposed root surfaces mostly in older patients New/Attacking Primary caries- lesions on unrestored surfaces Recurrent/secondary caries- lesions developing adjacent to restorations Speed of caries progression Acute Rapidly invading involving several teeth, untreated can result in pulp exposure, soft consistency, light coloured Chronic Slowly progressing, long standing caries, hard in consistency + dark coloured Rampant Suddenly appearing, widespread + rapidly burrowing, early involvement of the pulp, affecting those teeth that are regarded immune to caries. Arrested Caries that have become stationary/static No further progression, e’g occlusal surface with a large cavity which no longer retains food + becomes self-cleansing, marked brown pigmentation. Speed of caries progression Treatment + Restoration design Class I-Pit + fissure caries occur in the occlusal surfaces of pm + molars Class II- Proximal surfaces of pm and molars Class III-proximal surfaces of anterior teeth Class IV-proximal surfaces of anterior teeth involving the incisal edge Class V-Gingival third of facial/buccal+ lingual/palatal surfaces of all teeth Class VI-incisal edges of anterior and cusp tips of posterior teeth without involving any other ssurafce Treatment + Restoration design Pathway of caries spread Forward caries Caries cone in enamel is large or of the same size as dentine Backward caries Spread of caries along DEJ exceeds the caries in contiguous enamel Backward spread Extent of caries Incipient “white spot”, first evidence of caries activity, it consists of demineralized enamel, not extended to DEJ, the lesion can be remineralized, reversible caries. Occult Patients with a low caries rate, increased fluoride exposure, encourages remineralization of the surface enamel, whilst cavitation in dentine, the lesion gets masked by relatively intact enamel Cavitated Caries extends beyond the enamel into dentine, cannot be remineralized, irreversible caries Number of tooth surfaces Simple- one tooth surface Compound-two surfaces Complex-more than two surfaces Chronology Early childhood caries-Young children, characteristic with the four maxillary deciduous incisor teeth Adolescent caries- Variant of rampant caries, teenagers, presence of large pulp may increase pulp exposure Adult caries- Recession of gingiva + decreased salivary function, root caries are commonly seen the age of 55-60 years. Tooth surface to be restored Occlussal Mesial Distal Facial/labial Buccal Lingual/palatal Completely removed/not during treatment Residual caries- caries left in a prepared cavity even after restoration has been completed, intention/neglect Neglect-unacceptable Intentional- deep carious management to avoid pulp xposure WHO system Shape + depth of the carious lesion D1 – Clinically detectable enamel lesion D2- Clinically detectable cavities in enamel D3-Clinically detectable cavities in dentine D4- Lesion extending into the pulp Radiographic classification Incipient- caries involving less than half the thickness of enamel Moderate-caries involving more than half the thickness of enamel + do not involve the DEJ Advanced-Caries involving the enamel +DEJ + less than half the distance to the pulp Severe-caries involving dentine more than half the distance to the pulp cavity Graham + Mount classification Location of carious lesion Size of carious lesion Classification system used at UWC -criteria Modified American Dental Association Caries Classification System Tooth involved Surfaces Origin of lesion/anatomical site Extent of the lesion Activity of the lesion Histopathology of dental caries Enamel Dentine Incipient enamel caries Cavitation Zones of enamel caries Zones of dentinal caries Enamel caries Caries begins once the bacterial plaque gets deposited in the pits and fissures. Starts on the lateral walls of the tissues which eventually fuse at the base of the fissure. Later these pits and fissures become storehouse of bacteria causing dissolution of the remaining enamel and later spread of caries in dentin. Incipient lesion- these are covered with dental plaque. When the plaque is removed, the tooth dried, it appears opaque and turns translucent on wetting Cavitation- if the enamel lesion advances further, demineralization progresses resulting in cavitation Zones of enamel caries Surface zone Is least affected by caries Greater resistance due to greater degree of mineralization+ fluoride Less than 5% porous Radiopacity is comparable to adjacent enamel Zones of enamel caries Body of the lesion Largest portion of the incipient caries Found between the surface and the dark zone It is the area of greatest demineralization making it more porous Zones of enamel caries Dark zone Lies adjacent and superficial to the translucent zone It does not transmit polarized light Formed due to demineralization Zones of enamel caries Translucent zone Represents the advancing front of the lesion More porous than sound enamel Not always present Dentinal caries When the enamel caries reached the dentino-enamel junction (DEJ) it spreads rapidly laterally Least resistant to caries The spread of caries is more in demine as a result decreased calcification + the dentinal tubules act as a tract along which microorganisms travel to the pulp. Zones of dentinal caries Caries in dentine form a triangular shape with the base towards DEJ and apex towards the pulp with 5 distinct zones Zones of dentinal caries Zone 1 Normal dentine It is the deepest layer with normal collagen, odontoblastic processes and intertubular dentine Zones of dentinal caries Zone 2 Sub transparent dentine Inter-tubular dentine is demineralized There is no bacteria in this zone This zone is capable of remineralization Zones of dentinal caries Zone 3 Transparent dentine No bacteria Collagen crosslinking is intact This zone is capable of remineralisation Zones of dentinal caries Zone 4 Turbid dentine Dentinal tubules contain bacteria Here the dentine is not selfrepairable because of less mineral content Zones of dentinal caries Zone 5 Infected dentine Outermost zone Consists of decomposed dentine filled with bacteria Differences between infected + affected dentine Infected Affected Soft, demineralized dentine invaded with bacteria Soft, leathery, which can be flaked easily Irreversible denaturation of collagen, Cannot be re-mineralized Caries detecting dyes can stain Demineralized dentine but not invaded by bacteria Does not flake easily Uninterrupted collagen crosslinking Can be re-mineralized Does not stain DIAGNOSIS-how to detect dental caries Visual examination Tactile examination Radiographic examination Ultraviolet illumination Visual examination Based on the criteria like cavitation, roughness, opacification, discolouration of clean dried teeth under an adequate light source Tactile sensation An explorer is used to detect softened tooth structure Gentle pressure E.g of the pressure just blanching the fingernail without causing pain Radiographic examination Conventional intraoral periapical, bitewing radiographs are used Bitewing radiographs are used to detect interproximal caries Root carries appears as diffuse radiolucent areas with ill defend borders on proximal aspects of teeth in cervical areas Ultraviolet examination Natural fluorescence of enamel is decreased in carious areas because of less mineral content Carious lesion will appear as a dark shadow/spot against a fluorescent background. Recent methods of caries detection Digital dental radiography Digital imaging fiberoptic transillumination CARIES RISK ASSESSMENT The assessment of caries risk at screening or initiation of therapy allows for the following Better appraisal of caries activity Refinement of the treatment planning For e.g children at high risk will require intense prevention to primarily prevent caries initiation + secondarily to arrest caries progression Caries risk assessment High caries risk One new lesion on smooth surface during the past 1 year New carious lesion on the root surface Patient on medication which causes hyposalivation Systemic disorder Past dental history with multiple restorations Exposure to sugary snacks for more that three times a day Senility Caries risk assessment Status of the oral hygiene Poor oral hygiene, Non-fluoridated tooth paste, Low frequency of tooth cleaning, Orthodontic treatment, Partial dentures Dental history History of multiple restorations, Frequent replacement of restorations Medical factors Medications causing Xerostomia, Gastric reflux, Sugar-containing medications, Sjogrens syndrome Behavioural factors Bottlefeeding at night, Eating disorders, Frequent intake of snacks, More sugary foods, non-fluoridated toothpaste uasge Socioeconomic factors Low education status, Poverty, No fluoride supplememt PREVENTION Dietary measures Oral Hygiene Chemical measures Fluoride products Prevention: Dietary measures Avoid excessive intake of sugary + sticky foods Intake of raw fruits + vegetables helps in increase saliva flow, removal of food debris Fats form a protective bacteria on enamel or carbohydrates surface less available for bacteria Prevention: Oral Hygiene Can be maintained by toothbrushing, interdental cleaning by dental tape, floss, interdental brushes Prevention: Chemical measures Chlorohexidine gluconate: Binds to the bacterial cell wall+ interferes with membrane transport systems Fluorides: Ions increase the resistance of hydroxyapatite in enamel + dentine to dissolution by plaque acids Fluorides: formation of fluorapatite, Induces remineralization + inhibits bacterial metabolism Fluoride products: Professional topical fluorides are 2,72% acidulated phosphate (12 300 ppm fluoride) fluoride (APF) gel + 2% Sodium flouride gel (9 200 ppm fluoride) Fluoride Products: Flouride varnish, Mouthrinses + dentrifices REFERENCES Garg Nisha and Garg Amit 2020 Textbook of Operative Dentistry 4th ed. Jaypee Brothers Medical Publishers (P) LtD Garg Nisha and Garg Amit 2022 Textbook of Preclinical Conservative Dentistry 3rd ed. Jaypee Brothers Medical Publishers (P) LtD