Caries - Dr. Nermine El Bahey (4).pdf

DENTAL CARIES Dr. Nermine El Bahey 1  DENTAL CARIES C Dr. Nermine El Bahey Lecturer of Oral Pathology Pharos University Dr. Nermine El Bahey 2 Definition: Dental ca...

DENTAL CARIES Dr. Nermine El Bahey 1  DENTAL CARIES C Dr. Nermine El Bahey Lecturer of Oral Pathology Pharos University Dr. Nermine El Bahey 2 Definition: Dental caries may be defined as the progressive irreversible bacterial damage to the teeth, characterized by tooth demineralization (the inorganic substance & the organic matrix) through bacterial acids. Dr. Nermine El Bahey 3 Location of Dental Caries: ØMaxillary and mandibular first molars mostly affected. ØMandibular incisors are the most resistant to dental caries. ØThe occlusal surface is the most affected surface. Dr. Nermine El Bahey 4 Clinical appearance Earliest evidence is a chalky white etch on the translucent enamel which becomes softer than the sound enamel. Radiographically Caries usually appears radiolucent (interproximal). Dr. Nermine El Bahey 5 Dr. Nermine El Bahey ٦ Dr. Nermine El Bahey 7 Etiology of dental caries In 1890, Miller concluded that caries could result from decalcification caused by the bacterial acid production followed by invasion and destruction of any remaining tissue 'Acidogenic theory’. This theory proposes that the dietary carbohydrates are fermented by the oral bacteria leading to the formation of acid, which causes the progressive demineralization of the inorganic tooth substance, with the subsequent disintegration of the organic matrix. Dr. Nermine El Bahey 8 Dr. Nermine El Bahey 9 Factors contributing to Dental Caries: Other factors are: Dental Plaque and Saliva. Dr. Nermine El Bahey 10  Etiological Variables Factors Factors intrinsic to the extrinsic to tooth the tooth Dr. Nermine El Bahey 11  A. Role of Susceptible tooth Surface Tooth position Malaligned, posterior and crowded teeth retention of food debris and plaque. Tooth morphology Deep, narrow pits and fissures and below approximal contact favour the retention of food debris and thus plaque accumulation, resulting in increased caries susceptibility. Dr. Nermine El Bahey 12 Dr. Nermine El Bahey 13  A. Role of Susceptible tooth Surface Enamel structure Enamel hypoplasia and enamel hypocalcification may affect the rate of progression but not the initiation of caries. Newly erupted teeth are more susceptible to dental caries and their resistance increases due to hypermineralization and increase of the fluoride content. Dr. Nermine El Bahey 14 Dr. Nermine El Bahey 15  A. Role of Susceptible tooth Surface Enamel composition (Fluoride): The increase of fluoride content increases resistance to caries. During development it is incorporated in the tooth structure. Fluoride supply is found in: 1-Water. 2-Drinks (tea). 3-Food (sea food). 4-Therapy (topical application of fluoride). Thus, fluoride concentration increases on the outer tooth surface after tooth eruption. Dr. Nermine El Bahey 16 Mechanism of action of fluoride: It has a cariostatic effect which is thought to be mediated through: 1-Increasing enamel resistance to demineralization. 2-Enhancement of remineralization process of a carious lesion (repair). 3-Inhibition of bacterial growth (it inhibits bacterial enzymes and thus stops its activity. N.B. Increased fluoride more than {1.2 ppm} in the drinking water leads to fluorosis (mottled enamel).  B. Role of Diet / Carbohydrates There is a direct relationship between fermentable carbohydrates (CHO) in the diet and dental caries. 1- Physical factors: primitive, raw & unrefined foods were less cariogenic than modern soft refined foods. 2-Type of carbohydrate: Monosaccharides (glucose & fructose) less cariogenic because they are easily washed away. Disaccharides (Sucrose & lactose) are significantly more cariogenic than other sugars. WHY??? It is cheap, of low molecular weight that can diffuse easily into dental plaque, it is broken down rapidly by bacteria producing acids. Polysaccharides (starch) are less cariogenic. Dr. Nermine El Bahey 18 B. Role of Diet / Carbohydrates Sucrose Extra-cellular Intracellular glucans polysaccharides Dr. Nermine El Bahey 19  3-Total amount of intake: increase intake increase cariogenicity. 4-Frequency of intake: increase intake at intervals (between meals) will cause increase activity. 5-Texture: More sticky CHO are slowly washed by saliva and remain longer on the tooth surface. Dr. Nermine El Bahey 20 C. The Role of Bacteria Certain types of micro-organisms are intimately associated with dental caries: Dr. Nermine El Bahey 21  Streptococci are essential especially Streptococcus mutans. C Important in the initiation of dental caries at the tooth surface (smooth surface). Dr. Nermine El Bahey 22  Lactobacilli may be important in the progression of dental caries, especially dentin caries, and can produce fissure caries. C They are less important in the initiation of caries but they may play a role in tooth destruction. (Progression of caries) Dr. Nermine El Bahey 23  Actinomyces have been associated with root caries. C Dr. Nermine El Bahey 24  The essential features of cariogenic bacteria are: 1.Acidogenic: have the ability to produce acid. 2.Aciduric: have the ability to survive at a pH as low as 4.2 3.They form large amounts of extra-cellular, sticky and insoluble glucan plaque matrix. 4.They are able to form and store intra-cellular polysaccharides. 5.They have a proteolytic property i.e. possess proteolytic enzymes that are capable of digesting protein matrix of the tooth structure. 6. They have attachment mechanisms to firmly adhere to the smooth tooth surface. Dr. Nermine El Bahey 25  D. The Role of Dental Plaque Definition “Plaque is a tenaciously adherent deposit that forms on the areas of food stagnation on the teeth”. (Biofilm) It consists of: ØBacteria: up to 60% to 70%by volume. ØAmorphous Matrix: Mucin: derived from the salivary mucoids. Glucans: extracellular bacterial polysaccharides Carbohydrates Inorganic Content: calcium, phosphate and fluoride Food debris, leucocytes and desquamated epithelial cells Dr. Nermine El Bahey 26 Clinically üDental plaque is a thin yellow film on the surface of the teeth. üIt becomes visible, particularly on the labial surface of incisors when tooth brushing is stopped for 12-24 hours. üWith time, it undergoes mineralization to form dental calculus. üPlaque cannot be removed by rinsing. It resists the friction of food during mastication and can only be readily removed by tooth brushing. Dr. Nermine El Bahey 27 Dr. Nermine El Bahey ٢٨  Stages of plaque formation Stage I ØDeposition of the acquired dental pellicle. This a structureless, cell-free layer of salivary glycoproteins adsorbed on the tooth surface (3µ in thickness. ØIt is not usually visible to the naked eye. Dr. Nermine El Bahey 29 Stage II ØColonization of the acquired pellicle by bacterial flora, particularly by streptococcal strains. Stage III ØProgressive build-up and maturation of the dental plaque substance takes place by the proliferation of the heterogeneous flora. Dr. Nermine El Bahey 30 Proliferation of the heterogeneous flora. Anaerobic filamentous micro-organisms grow in long interlacing threads on which smaller bacilli & cocci become entrapped giving the corn-cob appearance  proliferation of Stages of Plaque Formation filamentous & other bact. Build up of plaque by bact.polisacarides Colonization of the cell free layer by BACTERIA specially S.M (24h.) Pellicle (cell free of salivary glycoprotein ) Dr. Nermine El Bahey 32 Factors Affecting Plaque Formation Anatomy and position of the tooth. Presence of prosthetic or orthodontic appliances. Structure of the tooth surface. Friction from diet and muscle movement during mastication. Oral Hygiene procedures. Diet composition. Dr. Nermine El Bahey 33  The role of the Plaque matrix: Retain acid in a high concentration at a particular site thus, allowing the demineralization of enamel. Slowing down the arrival of the salivary buffers from saliva thus delaying their neutralizing action and allowing the liberation of the mineral ions from the hyroxyapatite crystals and their diffusion into the plaque. Has an adhesive effect to the tooth surface. Dr. Nermine El Bahey 34 Acid production in the plaque: (Stephen Curve) It has been shown that after rinsing the mouth with 10% glucose solution, it diffuses rapidly into plaque and acid production quickly follows. the pH falls within 2-5 minutes, often to a level sufficient to decalcify enamel. Dr. Nermine El Bahey 35 §How Microbiological enzymatic reactions within the plaque lead to the carious attack on enamel ? Bacterial enzymes Lactic acid, Break them Break them into into Acetic acid Dietary sugars propionic acids ØAcid produced in the plaque contributes to a rapid fall in its pH value by as much as 2 units within 10 minutes after the ingestion of sugar. vAt a critical pH [about5.5] the acid attacks Enamel where mineral ions are liberated from hydroxyapatite crystals of the surface enamel and diffuse into the plaque. ØResulting in the liberation of the mineral ions from the hyroxyapatite crystals and their diffusion into the plaque Acid production in the plaque: 1. Sucrose diffuses rapidly into plaque & acid production quickly follows. 2. pH falls within 2-5 minutes to a level sufficient to decalcify enamel. 3. pH level remains at a low level about 15-20 minutes. 4. Over the next 30 to 60 minutes the pH slowly rises gradually to its original level. 5. These changes are known as : Stephen curve  Around a neutral pH, the plaque is supersaturated with mineral ions because of the extra ions from the enamel. Some of the excess ions in the plaque and may redeposited on the enamel crystal surface Therefore, there is a see-sawing of ions across the plaque enamel interface as the chemical environment within the plaque changes. Dr. Nermine El Bahey 38 §When periods of demineralization exceed those of remineralization, caries is produced. §When periods of remineralization exceed the those of demineralization, the lesion becomes resistant and arrested caries is produced. This occurs when sugar intake stops and oral hygiene is established by good tooth brushing. §The pH in the plaque falls rapidly but slowly gets back to the resting level!!! Dr. Nermine El Bahey 39 Dr. Nermine El Bahey 40  E. Role of Saliva: 1. Effect of Xerostomia 2. Rate of flow & buffering 3. Salivary viscosity 4. Salivary composition 5. Enzymatic & antibacterial activities 6. Immunopathological defense Dr. Nermine El Bahey 41  E. Role of Saliva: 1. Washing effect of SALIVA Rate of Flow Sialorrhea is accompanied by low caries activity (as in mongolism). Xerostomia, as in case of salivary gland aplsia and Sjogren’s Syndrome (xerostomia), is associated with an increased caries activity. Salivary Viscosity The higher the viscosity of saliva, the more is the caries incidence. Dr. Nermine El Bahey 42 2. Buffering capacity The normal salivary pH is neutral [7.2] or slightly alkaline, a low pH accelerates the demineralization of enamel. The buffering power of saliva depends upon its bicarbonate content and also the high ammonia and urea levels in saliva which retard the plaque formation and neutralize acids. Dr. Nermine El Bahey 43 3. Inorganic Components Availability of calcium phosphate and fluoride ions in saliva are essential for the re-mineralization process, where the calcium and phosphate ions are exchanged between the enamel surface and saliva. 4. Presence of antibacterial agents Such as lactoferrin and lyzosymes, but they have little significant effect on caries. Dr. Nermine El Bahey 44  5. Salivary Immunoglobulin Saliva contains secretory immunoglobulins A (SIgA). It is produced by plasma cells found in salivary glands. The main role of (SIgA)is: 1-killing of bacteria. 2-inhibition of its metabolic activity. 3-prevents adherence of bacteria to tooth surface. 6. Salivary Glycoproteins: forms the acquired enamel pellicle. Dr. Nermine El Bahey 45 Clinical classification of dental caries I-According to its location/ site of attack: Pit & fissure caries Smooth surface caries Root caries Recurrent caries Dr. Nermine El Bahey 46 1. Pits and fissures Ø This occur on the occlusal surface of molars and premolars, on the buccal and lingual surfaces of molars and on the lingual surface of maxillary incisors. Ø Caries may be detected clinically by a brown or black discoloration of a fissure in which a probe catches. Ø The enamel directly bordering the pit or fissure may appears opaque bluish white as it becomes under mined by caries. Dr. Nermine El Bahey 47 Dr. Nermine El Bahey 48 Pits & Fissures Caries Dr. Nermine El Bahey 49 2. Smooth surfaces caries Ø This occurs on the proximal surfaces of all teeth and on the gingival third of the buccal and lingual aspects (cervical caries). Ø It begins below the contact area as a well-demarcated chalky- white discoloration of the enamel. This white spot may become pigmented (yellow or brown). Dr. Nermine El Bahey 50 Dr. Nermine El B Bah ahey ahey Bahey 51 Smooth Surface Caries Dr. Nermine El Bahey 52  Smooth surface caries The cavity is crescent in shape Dr. Nermine El Bahey ٥٣ Dr. Nermine El Bahey 54 3. Cemental root caries Ø This occurs when the root surface is exposed. Ø It is clinically diagnosed by a soft and brownish discoloration of the tissue. Ø Demineralization is rapid, followed by bacterial invasion along the exposed collagen fibers. Ø Fracture and loss of successive layers of cementum. The fractures are usually parallel to the root surface resulting in shallow and saucer-shaped cavity. Dr. Nermine El Bahey 55 Root Caries Dr. Nermine El Bahey 56 Root Surface Caries Dr. Nermine El Bahey 57 Dr. Nermine El Bahey 58 4. Recurrent caries Ø It occurs around the margins or at the base of a previously existing restoration. Dr. Nermine El Bahey 59 II-According to rate of attack: Acute or Rampant caries Slowly progressing caries (Chronic) Arrested caries Dr. Nermine El Bahey 60 ØAcute / Rampant caries: It is rapidly progressing caries with early involvement of the pulp. It often occurs in many or all of the erupted teeth on the surfaces normally considered immune to caries ØCommon in children & young adults as dentinal tubules are large ,opened. Dr. Nermine El Bahey 61 Dr. Nermine El Bahey 62 Dr. Nermine El Bahey 63 Rampant Caries Caries in a patient with impaired salivary function as result of radiation therapy Dr. Nermine El Bahey 64 Dr. Nermine El Bahey ٦٥  RAMPANT NURSING CARIES (BABY BOTTLE SYNDROME): Acute caries affecting many teeth especially the maxillary four incisors and first molars. Dr. Nermine El Bahey 66 ØChronic caries: ØSlowly progressing caries, may take several months before pulp involvement ØMore common in adults. ØThere is sufficient time for both sclerosis of dentinal tubules & secondary dentin formation. Dr. Nermine El Bahey 67 Dr. Nermine El Bahey 68 Chronic Caries progress slowly, black or brown colored cavity hard remaining dentine Dr. Nermine El Bahey 69  3.Arrested Caries : ØBecomes static with no tendency for further progression. ØAppears as a large open cavity. ØLack of food retention. ØCommon on the occlusal surface of the mandibular premolars & molars. N.B. mostly because of the re-mineralization which has occurred from the precipitation of ions from the saliva. Dr. Nermine El Bahey 70 Dr. Nermine El Bahey ٧١ Progression of Caries Dr. Nermine El Bahey 72 Dr. Nermine El Bahey 73  Pathology of Enamel Caries ØEnamel Caries develops in Four Phases: 1-Phase of initiation 2-Phase of bacterial invasion 3-Phase of destruction 4-Phase of secondary enamel caries Dr. Nermine El Bahey 74  The process of enamel caries is a dynamic one and initially consists of alternating phases of demineralization and re-mineralization rather than a continuous process of dissolution. Dr. Nermine El Bahey 75 In ground sections The initial lesion is conical in shape and consists of a series of zones. These zones reflect different degrees of deminerlization and re-mineralization in enamel. Dr. Nermine El Bahey 76 In ground sections Smooth surface caries Conical in shape with its apex towards the ADJ and its apex towards the outer surface following the direction of the enamel rods. In pit and fissure caries ØCone in shape with the base at ADJ, and the apex towards the outer surface following the direction of the enamel rods. ØThe same changes in both pit and fissure and smooth surface caries take place and the same zones are seen. Microscopic Features of Dental Caries Early Enamel caries Translucent zone Dark zone Body of the lesion Surface zone Dr. Nermine El Bahey ٧٨ 1- The Translucent zone : It is the first histological change at the advancing edge of the lesion. 2- The Dark zone : It is superficial to the translucent zone.. 3- Body of the lesion : is the largest of all zones, forming the bulk of the lesion. 4-Surface zone : The most superficial zone. However, cavitation is the loss of this layer, allowing bacteria to enter the lesion. 1- The Translucent zone It is more porous than normal E (1% by vol. normal 0.1%) as it has many sub-microscopic pores formed due to the initial demineralization. In this zone, the apatite crystals decline in diameter from the normal 35-40nm to 25-30nm (1.2%mineral loss). Dr. Nermine El Bahey 80 2- The Dark zone It is superficial to the translucent zone. Pores constitute 2-4% by volume of this zone. Some pores are smaller than those of the translucent zone, suggesting that some re-mineralization has occurred due to the precipitiation of minerals lost from the translucent zone. Dr. Nermine El Bahey 81 3- Body of the lesion This zone is superficial to the dark zone and is the largest of all zones, forming the bulk of the lesion. It is recognizable clinically as the ‘brown spot’. This staining may be attributed to the exogenous pigments from food, tobacco and bacteria. Dr. Nermine El Bahey 82  There is more demineralization here, which leads to the formation of more pores (5-25%). It also contains apatite crystals that are larger than those of normal E. It is suggested that these large crystals result from the re-precipitation of minerals from the deeper zones. Dr. Nermine El Bahey 83 4-Surface zone This is the most superficial zone. It is about 40mm thick. It shows surprisingly little change in early lesions, as it has the highest mineral content of all zones. Therefore, it remains relatively normal despite the subsurface loss of mineral, this is because it is an area of active re-precipitation of minerals derived from both plaque and saliva, as well as from the dissolved deeper layers of the lesion as ions diffuse outwards. However, cavitation is the loss of this layer, allowing bacteria to enter the lesion. Dr. Nermine El Bahey 84  Cavity Formation At the (ADJ), caries spreads laterally to undermine the E. giving the bluish-white appearance. Ø Spread of bacteria along the ADJ, allowing them to attack the D. over a wide area. Ø Enamel loses its support of Dentine.  1 2 3 2 3 4 4 1.1.. Surface Zone Intact surface,