Understanding Oral Pathology - Dental Caries PDF

Understanding Oral Pathology Chapter 1 Dental Caries Lecture Notes for Students  Dental Caries Glossary Term...

Understanding Oral Pathology Chapter 1 Dental Caries Lecture Notes for Students  Dental Caries Glossary Term Meaning cariogenic causing tooth decay ‫مسبب للتسوس‬ a compound containing a ligand bonded to a central metal atom at two chelate/chelation or more points ‫ماسك‬ consumed ingested ‫مستهلك‬ criminal a person who had committed a crime ‫مجرم‬ enhances increases or intensifies the value or extent of something ‫يعزز‬ liberated freed, released ‫يحرر‬ pioneers the first to explore or settle a new place ‫رائد‬ the process of removing impurities or unwanted elements from a refinement substance ‫ تحسين‬،‫تنقية شوائب‬ susceptible prone to ‫عرضة إلى‬ tenacious persistent, clinging or adhering closely to ‫متمسك بشدة‬ texture the feel, appearance, or consistency of a substance ‫ بنية‬،‫ملمس‬ viscous sticky ‫لزج‬ 1  Dental Caries Chapter Outline I. Definition of dental caries II. Types III. Etiology (Factors affecting caries production) 1. Host factors: a) Susceptible tooth b) Saliva 2. Carbohydrates: a) Type of carbohydrate b) Amount of intake c) Frequency d) consistency and texture e) Local effect f) Refinement ** Experiment to demonstrate the role of carbohydrates in caries development 3. Cariogenic microorganisms: a) Criteria of cariogenic bacteria b) Types: - Streptococcus mutans - Lactobacilli ** Experiments to demonstrate the role of cariogenic microorganisms in caries development IV. Dental plaque: 1. Role 2. Mechanism of formation 3. Factors affecting carcinogenicity of dental plaque 4. Acid production in dental plaque ** Experiments to demonstrate the biochemical reactions occurring in bacterial plaque V. Demineralization and Remineralization of Enamel VI. Histopathology of Dental Caries 1. Histopathology of enamel caries 2. Histopathology of dentin caries VII. Root Caries VIII. Theories of Dental Caries 2  Dental Caries Dental Caries I. Definition Dental caries is a localized microbial disease affecting post eruptive hard tooth structures characterized by demineralization of the inorganic portion and destruction of the organic substance of the tooth. II. Types of caries A. According to site: 1. Pit and fissure caries 2. Smooth surface caries 3. Root caries B. According to stage: 1. Stage of spot (Incipient) 2. Enamel caries (Moderate) 3. Dentin caries (Advanced) 4. Deep dentin caries (Severe) 3  Dental Caries C. According to progression rate: III. Etiology of Dental Caries (Factors affecting caries production) Contributing etiological factors to dental caries (Newburn, 1982) i. Susceptible Tooth and Saliva (Host) ii. Substrate (Fermentable Carbohydrate) iii. Cariogenic Bacteria (Agent) iv. Time 4  Dental Caries ➔In addition to means of localization of micro-organisms and substrate at site of attack on tooth surface (dental plaque). 1. Host Factors a) Susceptible tooth b) Saliva a) Susceptible tooth i. Position: Role of Susceptible tooth in Dental Caries Position Morphology Structure Fluorides Genetic factors ii. Morphology Pits and fissures are much more susceptible to caries than the smooth tooth surface. This is because they are more difficult to clean. Their shape and depth determine the degree of caries susceptibility. Deep and narrow pits and fissures are more prone to decay than wide and shallow pits. Contact areas: Proximal lesions develop between contacting proximal surfaces (just below the contacting point) of two adjacent teeth. These areas are favorable sites for food retention and stagnation. 5  Dental Caries In young people, the contact points of recently erupted teeth are true contact points. In adults, after many years of small and frequent movements, wearing-off of the contact point results in a broad and flat contact area. 6  Dental Caries iii. Structure: iv. Fluorides: The increase in fluoride content in tooth increases its resistance to dental caries. Fluoride supply: o Water, which should not exceed 1.5 parts per million. o Drinks, as tea. o Food, as seafood. o Therapy, as topical application of fluoride. Mechanism of action of fluoride: Three main actions: a) Increasing enamel resistance to demineralization: Fluoride replaces the hydroxyl group in the hydroxyapatite forming fluorapatite which is less soluble in acids. b) Enhances remineralization. c) Inhibits bacterial growth: Fluoride inhibits bacterial enzymes. 7  Dental Caries v. Genetic Factors: Favorable or unfavorable tooth morphology is genetically inherited. Patients with Down syndrome have low caries index because of teeth spacing due to true generalized microdontia in permanent dentition, shallow fissures and higher salivary pH. Environmental factors as food habits and regular dental care acquired from family have decreases caries index in unfavorable teeth morphology. Remember conditions b) Saliva which cause Xerostomia. i. Washing effect Flow rate: increase in salivary flow rate decreases caries incidence and vice versa. Caries incidence increases in medical conditions causing xerostomia as in Sjogren syndrome and as a side effect to some drugs. Caries incidence is decreased in medical conditions such as in sialorrhea. ii. Salivary glycoproteins (degree of viscosity) Viscous saliva has a lowered washing effect; so saliva with low viscosity provides low caries incidence and vice versa. Salivary glycoproteins form the acquired enamel pellicle, which initially protects the enamel surface from being colonized by oral bacteria. iii. Buffering capacity Saliva has a bicarbonate/phosphate system neutralizes the pH fall (acidity) which occurs when bacteria metabolize sugar. Increase in buffers decreases caries incidence and vice versa. If the pH in the oral cavity is neutral (pH 7), or higher, this will help remineralizing enamel, and fights against the acidic effect of cariogenic bacteria. Similarly, by limiting the acidic foods in diet, an alkaline pH environment will be maintained. Foods which increases the oral pH (alkaline) such as: vegetables, beans, seeds. 8  Dental Caries Foods which decrease the oral pH (acidic) such as: carbohydrates, sugars coffee, dairy products, mustard and ketchup. iv. Antibacterial effect Lactoferrin: iron-binding protein interfering with bacterial iron metabolism. Peroxidase: inhibits streptococci and lactobacilli sIgA: inhibits bacterial adherence and prevents colonization of bacteria. Lysozyme: causes lysis to the bacterial cell wall 2. Role of Fermentable Carbohydrates (Substrate) Factors affecting cariogenicity of carbohydrates: i. Types of carbohydrates Monosaccharides Less cariogenic than disaccharides (glucose & fructose) since they are easily washed away Disaccharides Most cariogenic (sucrose, maltose & carbohydrate* lactose) Polysaccharides Least cariogenic of (Starch & glycogen) carbohydrates** 9  Dental Caries * Disaccharides are the most cariogenic carbohydrates, sucrose, in particular, has been described as the arch criminal of dental caries. This is because: 1- Sucrose is cheap, available in many forms and most frequently consumed carbohydrate. 2- It is of low molecular weight and can thus diffuse easily into dental plaque. 3- Sucrose is rapidly broken down by bacterial enzymes to produce acids. 4- The energy liberated from the break of the Role of Fermentable disaccharide bond is used by cariogenic bacteria to Carbohydrates in Dental produce dextran and levan. Caries ** Polysaccharides (starch, glycogen and cellulose) Types of carbohydrates Total amount of are less cariogenic because: carbohydrate intake Frequency of carbohydrate 1- They are of high molecular weight and cannot intake Texture and consistency of diffuse rapidly into plaque. carbohydrate 2- Not easily metabolized by oral bacteria, since Local effect of carbohydrate Refinement of carbohydrate breaking down of polysaccharides into simple Vipeholm experiment sugars by amylase in the saliva is a slow process. ii- Total Amount of Carbohydrate Intake  amount of CHO intake →  caries activity Example in USA and Europe.  amount of CHO intake →  caries activity Example Eskimos and during World War II 10  Dental Caries iii- Frequency of Intake of Carbohydrate Frequent intake of CHO, increases caries susceptibility because: 1- increases periods of availability of the CHO in the oral cavity. 2- increases periods of micro-organisms activity producing more acids (prolonged periods of low pH) 3- increases periods of acid demineralization to tooth structure. 4- Cleansing effect of other fibrous food elements is absent. iv- Texture of carbohydrate Sticky carbohydrate is more cariogenic because: 1. It remains for a long time in the oral cavity in relation to tooth surface. 2. It is slowly washed by saliva. 3. It is more accessible to micro-organisms to produce acids. v- Local effect of carbohydrate Carbohydrates should be introduced through the oral cavity (not directly into the stomach via a stomach tube) to be able to produce dental caries. vi- Refinement of Carbohydrate Definition: It is the treatment of raw carbohydrate (e.g. sugar cane) in industry to produce a refined sugar that is: -whiter -sweeter -remove fibrous material -improve flavour Refinement of carbohydrates increases cariogenicity because: 1- increase concentration of fermentable fraction of carbohydrate 2- increase adhesiveness 3- removal of fibrous material 11  Dental Caries Experiment to Demonstrate the Role of Carbohydrates in Caries Development Vipeholm Experiment (1945-1953) Aim: to investigate the effect of (i) amount, (ii) frequency of intake and (iii) texture of carbohydrates (stickiness) on dental caries susceptibility. Material & Methods: The experiment was conducted in Vipeholm Hospital which is an institute for the mentally deficient in Sweden. 12  Dental Caries patients were divided into 7 groups according to the given diet one control group (free from refined sugar) and 6 test groups The Six main test groups were: Carbohydrate solution Sweetened bread at meal time Chocolate at meal times Caramel between meals Toffee at meal times & between meals Toffee between meals Caries index was calculated for each individual by the DMF index [D (decayed) M (missing) F (filled)] Conclusion Increase in sugar consumption increases caries activity. Risk is greater if consumed in a form that stays on tooth surface (sticky) for longer time. Increased risk of caries activity if CHO are consumed between meals. Therefore, frequency and texture of carbohydrates are more effective on caries activity than total amount of carbohydrates 13  Dental Caries Sucrose is the arch criminal of dental caries. ❖ Sucrose with the help of cariogenic bacteria (S. mutans) plays an active role in building of bacterial plaque forming extracellular polysaccharides. What is the difference between Dextran and Levan? Dextran Levan Extracellular polysaccharide Extracellular polysaccharide Glucose polymer Fructose polymer Water insoluble Water soluble Highly adhesive and sticky Less adhesive and less sticky Resist degradation Rapidly broken and lost within Provides bulk of dental plaque few hours Act as store for CHO 14  Dental Caries 3. Role of Bacteria in Dental Caries Cariogenic bacteria produce acids that lead to the demineralization of enamel and dentin. Experiments to Demonstrate the Role of Cariogenic microorganisms in Caries Development I. Miller’s Experiment (1890) Miller proposed that dental caries development was dependent on the presence and proliferation of cariogenic microorganisms. He suggested that bacteria produced acids that led to the demineralization of enamel and dentin. Experiment: Miller suspended 2 sound teeth in 2 test tubes containing fermentable carbohydrate and saliva (which contains microorganisms). One of the tubes was boiled (to kill the microorganisms), then both tubes were incubated at 37 0C. After a certain time, ONLY the tooth suspended in the tube which was not boiled showed caries-like lesions. 15  Dental Caries II. Orland’s Experiment (1954) Orland and colleagues showed that rats fed a diet which is normally cariogenic failed to develop dental decay in the absence of bacteria. Orland's experiments to produce Germ-free and Gnotobiote animals: 1- Production of Germ-free animals: Aim: Is bacteria essential for production of dental caries? Material & Methods: i. A pregnant female rat was put in a sterile operating theatre to deliver her offspring under complete aseptic conditions. ii. A caesarian section was done, and the delivered rats were divided into two groups; a group was left in the aseptic 16  Dental Caries conditions (germ-free) and the other group was placed outside under ordinary life conditions. iii. Both groups were fed a cariogenic diet. Observation & Results: The group that was kept under aseptic conditions did not produce dental caries when compared to their siblings under normal life conditions. Conclusion: Bacteria is essential for production of dental caries. 2- Production of Gnotobiotes: Gnotobiote comes from the Greek vocabulary: ‘gnotos’: well known, ‘biota’: all life Definition of gnotobiote: an animal in which all the life forms (bacteria, viruses, fungi, protozoa and other saprophytes or parasites) are known. How did Orland and co-workers (1955) produce gnotobiotes: Aim: Do all bacteria similarly produce dental caries? Material & Methods: i. After the production of germ-free rats, they were divided into groups and fed cariogenic diets with ONE known strain of micro-organism (streptococci, staphylococci, lactobacilli, actinomyces, etc.). ii. The gnotobiote rats were isolated from each other for prevention of cross- contamination. Observation & Results: - After a period of time, the rats given the diet with streptococcus mutans produced smooth surface and pit and fissure caries. - The group that was fed cariogenic diet with lactobacilli produced pit and fissure caries only. - The other groups didn't produce dental caries. 17  Dental Caries Conclusion: 1- Not all bacteria produce dental caries. 2- Streptococcus mutans is more cariogenic than lactobacilli. What are the Essential Features for a Bacteria to be Cariogenic? The characteristic features of cariogenic bacteria include the following: Importance of Extracellular and Intracellular 1. Ability to produce acids = Acidogenic Polysaccharides 1- Extracellular 2. Ability to survive in an acidic environment = Aciduric polysaccharides afford a 3. Synthesis of insoluble extracellular polysaccharides means of adhesion to smooth tooth surfaces and glucans (dextrans) form the bulk of dental plaque. They also act as a 4. Synthesis and utilization of intracellular storage barrier to the diffusion of polysaccharides (amylopectin) acids from the plaque and the entry of salivary buffers 5. Ability to actively transport fermentable sugars into plaque. when in competition with other plaque bacteria 2- Intracellular polysaccharides, on the even against a concentration gradient other hand, provide additional source of 6. Have attachment mechanisms for firm adhesion to fermentable carbohydrate tooth surfaces after dietary carbohydrate has been cleared away. CARIOGENIC BACTERIA 1) Streptococcus mutans 1. Named mutants because of its varying morphology. They undergo mutation in their morphology by changing their shape from round to rod under different environmental conditions like decrease in pH. 18  Dental Caries 2. They are closely associated with the initiation of caries in humans, because they have the ability to synthesize extracellular polysaccharides dextran and levan. Dextrans, are insoluble and adhesive sticky substances enabling micro-organisms to adhere to smooth tooth surface and to other microorganisms (i.e. having attachment mechanisms). 3. They are transmissible from one individual to another 4. Able to ferment a variety of sugars, i.e. they are acidogenic 5. Very acid tolerant; can live at a low pH of 4.2 (aciduric) 6. They are capable of producing intracellular polysaccharides (amylopectin). Amylopectin is made up of glucose and act as a store of fermentable carbohydrate when there is deficiency of dietary carbohydrate intake. 7. It adheres to plaque pellicle by Adhesins 2) Lactobacillus species 1. Lactobacilli are: ▪ Acidogenic ▪ Aciduric can live at a low pH of 3.5 2. Lactobacilli can produce pit & fissure caries only in gnotobiote animals. They can’t produce extracellular or intracellular polysaccharides thus they cannot attach themselves to the smooth surfaces of the teeth. 3. They do not play an important role in the initiation of dental caries, though they play a role in its progression. 4. They have been isolated from carious dentin and are considered as pioneer organisms in dentine caries 5. The lactobacilli count was once used as an index of caries activity as it was observed that lactobacilli are present in large numbers in saliva in persons with high caries activity. 3) Actinomyces Viscosus is involved in root caries 19  Dental Caries IV. Dental plaque (Role of Bacterial Plaque in Dental Caries) Role of Bacterial Plaque in Definition: Dental Caries Dental plaque is a tenacious biofilm formed Definition on tooth surfaces when tooth brushing is Composition Clinical appearance stopped for 12-24 hours. Mechanism of formation It is formed of: Role of plaque matrix Factors affecting plaque formation Acid production in plaque Biochemical reactions in the dental plaque 20  Dental Caries Mechanism of formation of dental plaque Mechanism of formation of dental Plaque 1) Formation of an acquired enamel pellicle 2) Colonization of cell-free pellicle by bacteria (formation of dental plaque) a. Initiation of a pioneer community b. Formation of an intermediate community c. Establishment of a mature community 1) Formation of an acquired enamel pellicle Acquired Enamel Pellicle is an acellular, structureless, organic, bacteria-free film of salivary glycoproteins that coats the enamel surface when a thoroughly cleaned tooth is exposed to saliva. It is formed by selective adsorption of certain salivary glycoproteins via electric charges on the apatite crystal. This formation is the first step of plaque development. Later, this layer is colonized by bacteria that adhere to the pellicle. Acquired enamel pellicle is 0.1-1.0 µm thick. Colonization of cell-free pellicle by bacteria is in THREE WAVES I. Initial Community 1- Colonization phase (8 hours): Primary colonizers (pioneers): S. viscosus and S. sanguis. They bind to the pellicle. 2- Rapid growth phase (8-48 hours): bacteria spread as a monolayer and then palisade perpendicular on the tooth surface. 21  Dental Caries II. Intermediate Community (Secondary colonizers) – Streptococcus mutans attach to the established pioneer species where they ferment carbohydrates and produce lactic acid. – Extracellular polysaccharides produced by bacteria allow other organisms to attach to dental plaque III. Mature Community (Climax community) Filamentous organisms proliferate and predominate arranging themselves parallel to each other and at right angles to the tooth surface. This arrangement of distinctive bacterial aggregations is referred to “corn on the cobs.” By this time (after 8 days) a wide variety of organisms join the community including lactobacilli, actinomyces naeslundii and others Role of plaque matrix: 1. Acts as a diffusion-limiting membrane: a. retain the produced organic acid (lactic acid) in high concentrations to initiate caries activity. b. slows down the entry of buffers from saliva to delay their neutralizing action. 2. Contributes to adhesiveness, bulk and resistance to washing by saliva. 22  Dental Caries Acquired enamel pellicle formation 0-4 hr Attachment of single bacterial cells Growth of attached bacteria leading to 4-24 hr formation of distinct microcolonies 1-14 Microbial succession and co-aggregation days 2 weeks Climax community and mature plaque or older Factors affecting plaque formation: 1. Anatomy and position of tooth 2. Presence of appliances 3. Structure of tooth surface 4. Friction from the diet and masticatory movements 5. Oral hygiene measures 6. Composition of the diet (plaque forms more rapidly on high sugar diet) 23  Dental Caries Biochemical Reactions Occurring in Bacterial Plaque I. Stephan’s Experiment Biochemical Reactions Aim: Occurring in Bacterial Plaque Acid production (Stephan’s To prove the importance of acid production in experiment) dental plaque Formation of extracellular polysaccharides Material & Methods Formation of intracellular - He divided individuals into groups polysaccharides Demineralization phase according to caries activity. Remineralization phase - pH was recorded after two hours of the last meal (on a day during which no fermentable carbohydrates were consumed) and this pH is called resting pH - One micro-electrode was placed in contact with the developed plaque on teeth and another was placed in the floor of the mouth (saliva the electrolyte medium) - Individuals were asked to rinse their mouth for ten seconds with 25 ml. of 10% glucose. - The pH was recorded immediately, after two minutes, , after 5 min. and then every 10 min. - The pH values were plotted against time and a curve was produced called Stephan's curve. Observations - After CHO rinse  fall in pH within 2-5 min  to reach pH 5.5 (critical pH) - pH drops below 5.5 - pH remains at this level for about 10-30 min. - pH gradually returns to resting pH after about one hour - pH doesn’t return to the resting pH in caries active patients 24  Dental Caries Conclusions - After CHO rinse  rapid fall in pH occurs due to: 1- Rapid diffusion of sugar into dental plaque. 2- The activity of large numbers of bacteria and enzymes in the dental plaque. - Demineralization of enamel At critical pH = 5.5  Ca2+, PO4- are liberated from enamel hydroxyapatite crystals and diffuse through plaque. Liberated Ca++ are removed by a chelating action in the plaque leaving microspaces in the enamel structure - Remineralization phase: pH slowly increases to reach resting levels  plaque is supersaturated with Ca2+, PO4- so excess ions become 25  Dental Caries deposited on enamel surface. This occurs when the sugar intake stops, and by good tooth brushing (oral hygiene) The slow return in pH is due to: 1- The continued metabolism of residual sugar absorbed by the plaque. 2- The breakdown of reserve polysaccharides in the plaque. 3- The diffusion limiting property of dental plaque which results in: Delayed diffusion of salivary buffers into the plaque. Delayed diffusion of acids outwards into the saliva. V. Demineralization and Remineralization of Enamel (Chemistry of Enamel Caries) N.B. Dental caries is a dynamic process. It consists of periods of demineralization and periods of remineralization. When the periods of demineralization exceed those of remineralization then caries is produced. When the periods of remineralization are more than the periods of demineralization, the lesion becomes resistant and arrested caries is produced. 26  Dental Caries VI. PATHOLOGY OF DENTAL CARIES I. Macroscopic Appearance Appear as an opaque chalky white hard area ‘white spot’. White opaque spot forms adjacent to contact point. Slowly progressing caries appears as ‘brown spot’. A carious lesion is considered active when it shows more of these characteristics: it is whitish, matte, has a rough texture (when carefully touched with the tip of a blunt probe), has plaque stagnation, is cavitated, and if there is gingival bleeding. II. Microscopic Appearance 1. Histopathology of Enamel caries Permeation of enamel by acids cause a series of submicroscopic changes identified as separate zones with different chemical structure (mineral content). 27  Dental Caries Enamel caries develops in four main phases: i- Phase of initiation ii- Phase of bacterial invasion iii-Phase of destruction iv- Phase of secondary enamel caries i. Phase of initiation - The early lesion depends on the intensity of acid attack creating submicroscopic pores - In ground sections, the early smooth surface enamel caries lesion consists of four zones. 1) Translucent zone Located towards dentin and it is the deepest zone located on the advancing front. The name refers to its structure when perfused with quinoline solution and viewed with polarized light microscopy. The pores form along the enamel prism. When quinoline solution is mounted on the section, the submicroscopic pores become filled with it and the normal structural features are lost and this zone appears as translucent as enamel. Submicroscopic pores account for 0.1-1% of total enamel volume This zone represents initial demineralization. 2) Dark Zone Superficial to translucent zone Further demineralization takes place (nearer to the source of acid) 28  Dental Caries Early Enamel Carious Lesion Known as 'dark zone' because it does not transmit polarized light. This light blockage is caused by the presence of many tiny pores that are unable to absorb quinoline. The smaller pores may be due to remineralization which occurs in the larger pores in periods when there is no acid production. Submicroscopic pores account for 2 - 4% mineral loss of total enamel volume Radiolucent compared to previous zone and to enamel 3) Body of the Lesion Largest zone extending superficial to the dark zone and below the surface zone Increased pores with both large and small ones, 5% (at the periphery) - 25% (at the center of the lesion) mineral loss More radiolucent (alternating radiolucent and radio-opaque lines) Progressive demineralization. 29  Dental Caries 4) Surface Zone 25-30µ thick with decrease in pores, 1% mineral loss More radio-opaque than the deeper zones since it is more mineralized than the underlying body of the lesion. The surface remains intact and becomes hypermineralized in early enamel lesion. This is due to: i. The active reprecipitation of minerals derived from the plaque and from deeper layers of the lesion as dissolved minerals diffuses outwards. ii. Higher fluoride content from food and toothpaste containing fluoride or topical fluoride application. iii. Different crystal orientation. A: Surface zone appears intact; B: Body of the lesion; note the pronounced striae of Retzius C: Dark zone: surrounds the body of the lesion and is the zone where caries is in progress D: Translucent zone is seen surrounding the entire advancing front of the lesion 30  Dental Caries ii. Phase of Bacterial Invasion When sufficient pathways are created by the action of acids, central defects occur to hollow the crystal hexagons. As dissolution increases, disorganization of crystal arrangement occurs (pores become large enough after removal of sufficient amounts of Diagrammatic presentation of minerals by acids to allow the invasion of dissolution in enamel prisms bacteria). 31  Dental Caries iii. Phase of Destruction Loss of enamel minerals leads to loss of structure (90% by volume) Enamel The structural integrity of enamel is lost. The organic matter either collapses or is digested by the action of proteolytic bacteria Dentin (proteolytic enzymes) iv. Phase of Secondary Enamel Caries When the acids reach the dentino-enamel junction (DEJ), it spreads laterally. This lateral spread gives enamel the bluish-white appearance seen clinically. Three major effects of the lateral spread: 1- Enamel loses support of dentin and hence it is weakened (separation of enamel from dentine) 2- Reverse attack from beneath (secondary enamel caries) 3- Spread of acids followed by bacteria along DEJ which allows the attack of dentin over a wide area. 32  Dental Caries Bluish white discoloration of enamel due to underlying spread of carious lesion along amelo-dentinal junction 2. Histopathology of Dentine Caries What is Dentine? Mineral phase: consists of hydroxyapatite crystallites (about 75%) Organic phase: forms about 20% of dentine; mostly a dense network of insoluble collagen fibers and a little soluble protein Dentinal tubules: forms the bulk of the matrix Odontoblastic processes occupy the dentinal tubule starting from the odontoblasts in the pulp 33  Dental Caries Macroscopic Features The carious lesion is conical in shape due to the lateral spread of acids along the DEJ with its base towards enamel. Microscopic Features Develops after bacterial invasion occurs in enamel and a cavity is formed, i.e. surface of enamel is not intact. I. Uninfected Dentinal Lesion (acid attack): 1- Reactionary (or tertiary) dentine: The dentinal lesion -In response to odontoblast irritation, a layer of involves: reactionary (or tertiary) dentine is formed at the surface of the pulp chamber deep to the dentine I- Uninfected lesion caries. (deepest and most close to the pulp, -The tubules are irregular, tortuous, and fewer in caused by Acid Attack) number than in primary dentine. 1-Reactionary dentine -Its formation increases the depth of tissue 2-Zone of hypermineralization between the carious dentine and the pulp, and 3-Zone of demineralization delays involvement of the pulp. II- Infected dentinal lesion 2- Zone of sclerosis (Hypermineralization) 4-Bacterial Invasion -The sclerotic or translucent zone is located 5-Dentinal destruction beneath (pulpal) and at the sides of the carious (superficial zone) lesion. Sclerosed dentine has a higher mineral content. 34  Dental Caries -Sclerotic zones appear translucent when ground sections are seen by transmitted light. -Translucent dentine forms because of continuous deposition of calcium salts within the walls of dentinal tubules obliterating them. - Narrowing the diameter of the tubules protects deeper dentine and pulp against acid attack and bacterial invasion. NB: With rapid lesion progression and when subjected to excessive acid attack, the odontoblasts are destroyed without having produced dentinal sclerosis. These are called Dead tracts. The empty dentinal tubules contain air and the remains of the dead odontoblast process. These appear dark by transmitted light and translucent by reflected light. 35  Dental Caries 3-Zone of demineralization: Acid produced by bacteria diffuses ahead (in advance) of the bacterial front resulting in demineralized uninfected dentin. Minerals are removed from the inner walls of the tubules, which become wider, thus making a pathway for bacterial invasion. II. Infected Dentinal Lesion: Develops after bacterial invasion occurs in enamel and a cavity is formed, i.e. surface of enamel is not intact. 4- Zone of bacterial invasion: -In this zone the bacteria extend down and multiply within the dentinal tubules. -The bacterial invasion probably occurs in two waves: the first wave consisting of acidogenic organisms, mainly lactobacilli, producing acid. -A second wave of mixed acidogenic and proteolytic organisms then attack the demineralized matrix. -The walls of the tubules are softened by the proteolytic activity and may be distended by the increasing mass of multiplying bacteria. Proliferation of the microorganisms within the dentinal tubules results in adjacent beads, coalescing with each forming larger distended segments of dentinal tubules filled with microorganisms. Liquefaction foci are longitudinal in orientation, while transverse clefts are perpendicular to the dentinal tubules. 5- Zone of destruction - Neighboring liquefaction foci and transverse clefts coalesce with each other forming progressively larger and more irregular cavities filled with micro-organisms and debris. -The normal dentine architecture is lost. 36  Dental Caries 1. Uninfected dentinal lesion 2. Infected dentinal lesion 3. Dentinal destruction Transverse clefts are similar to the liquefaction foci in their content and are formed due to: 1- lateral branches of the dentinal tubules 2- less calcified areas in dentine as the interglobular spaces 3- along the incremental lines which represent resting phases of dentine and contain organic matter. 37  Dental Caries Uninfected Dentinal Lesion Infected Dentinal Lesion Bacteria is involved after widening of dentinal No bacteria is involved, acid attack only tubules and softening Collagen is reversibly denatured Collagen is irreversibly denatured Remineralizable and should be Not remineralizable and should be removed preserved Includes Zones of reparative dentine, Includes zone of bacterial invasion (beading, zone of hypermineralization (sclerosis, liquefaction foci and transverse clefts) and translucent dentine) and zone of superficial destruction zone. demineralization. 38  Dental Caries Diagrammatic representation of the zones in established dentine caries 39  Dental Caries Infected Affected VII. Root surface (cementum) Usually due to exposure of the neck of the tooth to the oral environment as a result of gingival recession (periodontal diseases or age changes). The exposed enamel-cementum junction is highly irregular and presents a bacterial retention site (mainly Actinomyces, S. mutans and lactobacilli). In contrast to early enamel caries the bacteria in the plaque on the root surface penetrate into the superficial layer of the demineralized cementum very early invading it along the exposed collagen fibers (Sharpey’s fibers). The basic reactions and carious destruction of root dentine is similar to that described for coronal caries. Likewise, reactive dentine is formed towards the pulp corresponding to the involved tubules. 40  Dental Caries IX. Theories of Dental Caries Proteolysis Chelation Proteolytic Theory Theory * A chelator is a molecule The Acidogenic Theory * suggests that the first that can bind a metal ion (Miller's Chemico- attack is by the action of in a claw-like parasitic Theory) proteolytic bacteria on configuration to form a *Most acceptable theory* the protein matrix of ring structure (chelas: Two stages: enamel. claw). * decalcification of *The organic structure *This theory suggests that enamel by the acids of enamel provides a proteolytic bacteria act derived from the pathway for invasion by on the organic matrix of fermentation of sugars bacteria. enamel liberating (decalcification by acidogenic bacteria) * Bacteria act on chelating agents to * followed by the sulfated transport the calcium ions dissolution of the mucopolysaccharides out of enamel at a neutral softened residue producing sulfuric acid pH or even in an alkaline which causes one. demineralization Proteolysis Chelation Proteolytic Theory Theory POINTS 1. It doesn't explain the 1. It does not explain the AGAINST role of carbohydrates in role of sugars in dental dental caries. caries. 2. Proteolytic bacteria 2. Proteolytic bacteria did failed to produce caries not produce caries in in gnotobiotes. gnotobiotes. 3. The amounts of acids 3. This theory suggests produced from the that caries occurs in a breakdown of the organic neutral medium rather matrix is too small to than an acidic one. demineralize enamel 41  Dental Caries Chapter Highlights Contributing etiological factors to dental caries are: susceptible tooth, saliva, substrate, cariogenic bacteria and time. The position of the tooth in the oral cavity affects its susceptibility to dental caries. The morphology of the tooth in the oral cavity affects its susceptibility to dental caries. Enamel hypoplasia and enamel hypocalcification may affect the rate of progression of the caries but not its initiation. Newly erupted teeth are more caries susceptible. Later the resistance of these teeth to caries increases due to post eruptive maturation. The increase in fluoride content in tooth increases its resistance to dental caries. There are three main actions of fluorides: increasing enamel resistance to demineralization, enhances remineralization and inhibits bacterial growth. Saliva has a washing effect and saliva with low viscosity provides low caries incidence and vice versa. Saliva has a bicarbonate/phosphate system which neutralizes the pH fall (acidity). Increase in buffers decreases caries incidence and vice versa. Cariogenicity of carbohydrates depends on the type of carbohydrate. Disaccharides are the most cariogenic carbohydrates. Total amount of carbohydrate intake as well as frequency of intake affects cariogenicity. Texture and refinement of carbohydrates also affects its cariogenicity. Vipeholm experiment aims to investigate the effect of (i) amount, (ii) frequency of intake and (iii) texture of carbohydrates (stickiness) on dental caries susceptibility. And it was concluded that increase in sugar consumption increases caries activity and that the risk is greater if consumed in a sticky form for a longer time. Sucrose is the arch criminal of dental caries. Dextran is an extracellular poly saccharide formed of glucose polymer which provides bulk to the dental plaque. Levan is an extracellular poly saccharide formed of fructose polymer which acts as a store for carbohydrates. 42  Dental Caries Miller proved that dental caries development was dependent on the presence and proliferation of cariogenic microorganisms. Orland showed that rats fed a diet which is normally cariogenic failed to develop dental decay in the absence of bacteria. Streptococcus mutans produce smooth surface and pit and fissure caries. They are closely associated with the initiation of dental caries. They are acidogenic and aciduric. Lactobacilli produce pit and fissure caries only. They are acidogenic and aciduric. They can’t produce extracellular or intracellular polysaccharides thus they cannot attach themselves to the smooth surfaces of the teeth. They do not play an important role in the initiation of dental caries, though they play a role in its progression. Dental plaque is a tenacious biofilm formed on tooth surfaces when tooth brushing is stopped for 12-24 hours. It’s mainly formed of microorganisms. Acquired Enamel Pellicle is an acellular, structureless, organic, bacteria-free film of salivary glycoproteins that coats the enamel surface. Initial Community: Starts with the colonization phase and then the bacteria spread as a monolayer and then palisade perpendicular on the tooth surface. Intermediate Community (Secondary colonizers): Strept. mutans attach to the established pioneer species. Strept. mutans ferment carbohydrates and produce lactic acid. This leads to an increase in the number of aciduric bacteria. Extracellular polysaccharides produced by bacteria allow other organisms to attach to dental plaque. Mature Community (Climax community): Filamentous organisms proliferate and predominate arranging themselves parallel to each other and at right angles to the tooth surface. This arrangement of distinctive bacterial aggregations is referred to “corn on the cobs.” Plaque matrix: Acts as a diffusion-limiting membrane and contributes to adhesiveness, bulk and resistance to washing by saliva. Stephan’s experiment was done to prove the importance of acid production in dental plaque and concluded that after carbohydrate rinse a rapid fall in pH occurs. The critical pH is equal to 5.5 and it is the pH at which demineralization of enamel starts. 43  Dental Caries In the phase of initiation of enamel caries, the early lesion depends on the intensity of acid attack creating submicroscopic pores. In ground sections it consists of four zones; translucent zone, dark zone, body of the lesion and surface zone. The surface remains intact in early enamel lesion. Phase of bacterial invasion occurs when sufficient pathways are created by the action of acids, which allows the invasion of bacteria. In the phase of destruction, 90% loss of structure occurs and the structural integrity of enamel is lost. The organic matter either collapses or is digested by the action of proteolytic bacteria. Phase of secondary enamel caries: When the acids reach the dentino-enamel junction (DEJ), it spreads laterally. Hence, enamel loses support of dentin and reverse attack from beneath takes place. The dentinal lesions involve uninfected lesion which is the deepest and close to the pulp and infected dentine lesion. In the uninfected dentine lesion, a layer of reactionary dentine is formed at the surface of the pulp chamber deep to the dentine caries, over whicha zone of sclerosis is seen. Dead tracts are also seen. In the infected dentine lesion, proliferation of the microorganisms within the dentinal tubules results in adjacent beads, coalescing with each forming larger distended segments of dentinal tubules filled with microorganisms. Liquefaction foci are longitudinal in orientation, while transverse clefts are perpendicular to the dentinal tubules. When neighboring liquefaction foci and transverse clefts coalesce with each other they form the zone of destruction which is filled with micro-organisms and debris. Root caries occurs due to gingival recession. The exposed enamel-cementum junction is highly irregular and presents a bacterial retention site. The acidogenic theory is the most accepted theory in dental caries. 44