Dental Caries (bacterial tooth loss)

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Information about Dental Caries (bacterial tooth loss)

Published on March 23, 2013

Author: nurved



At the end of this lecture, the student should be able to:
Develop understanding of the classification
Describe how a cyst develops.
Describe the origin and identifying characteristics of the radicular cyst.
Describe the origin and identifying characteristics of the Dentigerous cyst.
Describe the origin and identifying characteristics of the Odontogenic Keratocyst cyst.
Describe the radiographic characteristics of the dentigerous cyst and the odontogenic keratocyst.
Discuss the radiographic appearance of the lateral periodontal cyst. 8. List the factors involved in the nevoid basal cell carcinoma syndrome.
State the histologic finding that is a key diagnostic feature of Radicular, Dentigerous & Keratocysts.
Describe the origin and identifying characteristics of non odontogenic cysts.
Describe different treatment options available, and their clinical importance.

DENTAL CARIES Dr. Ali Yaldrum B.D.S, M.Sc (London)Faculty of Dentistry, SEGi University get in touch

Learning Objectives• Define “Dental Caries”• Describe classification of caries• Describe progression of caries in enamel• Describe progression of caries in dentin• Describe progression of caries in root surface• Analyze the fundamental differences of caries progression between enamel & dentin• Develop holistic understanding of the disease

Contents Click on the topic to jump1. Dental Caries (definition)2. Aetiology of Dental Caries 8. Reactionary Changes in3. Biological Events initiating Dentin caries 9. Root surface caries4. Pathology of Caries 10. Arrested Caries &5. Enamel Caries Remineralization6. Cavity Formation7. Caries in Dentine

Dental CariesIt is bacterial disease of calcified tissue ofthe teeth characterized by demineralizationof the inorganic and destruction of theorganic substance of the tooth

Saliva Caries Time SalivaSaliva Plaque Susceptible Bacteria Surface Sugar Saliva Aetiology of caries (fig.1)

Sugar Polysaccharides Plaque buffer Ca+Salivary ACIDSBuffers Ca+ Plaque buffer Polysaccharides Sugar Plaque Bacterial Enamel Enzymes Biological events initiating Dental Caries (fig.2)

Pathology of Dental Caries Dental caries can be classified into • Site of attack • Rate of attack

Site of Attack• pits or fissure carries: 1. Molars and premolar 2. Buccal and lingual surface of molars 3. Lingual surface of maxillary incisors

Site of Attack• Smooth surface caries: 1. Approximal surface (fig.3) 2. Gingival third of lingual and buccal surface 3. Choky white appearance of the enamel

nterprismatic substance havezonesdestroyed. The same appearance is features of these been are summarised in Table 3.2. een in chalky enamel caused by early caries. (By kind permission ofDr K Little.) The translucent zone is the first observable change. The appearance of the translucent zone results from formation of sub-e or microscopic spaces or pores apparently located at prism bounda- 3.19 Diagram summarising the main features of the precavitation Fig.mel, phase of enamel caries as indicated here in this final stage of acid attack ries and other junctional sites such as the striae of Retzius. Whenmost the section is mounted in quinoline, it fills the pores and, since enamel before bacterial invasion, decalcification of dentine has begun. on The area (A) would be radiolucent in a bite-wing film but the area (B) couldcon- it has the same refractive index as enamel, the normal structural visualised only in a section by polarised light microscopy or microradi- beack. features disappear and the appearance of the pores is enhanced ography. Clinically, the enamel would appear solid and intact but the sur- tine (Fig. 3.13). Microradiography confirms that the changes in the would be marked by an opaque white spot over the area (A) as seen face in Figure 3.11 (From McCracken AW, Cawson RA 1983 Clinical and oraleas- translucent zone are due to demineralisation. microbiology. McGraw-Hill.)tackper-e of t ofrys-e to ries s istingan ahese and ig. 3.18 The organic matrix of developing enamel. An electronphotomicro- pot) of a section across the lines of the prisms before calcification showing raph he matrix to be3.11 dense in thecaries, aof the prism sheaths than in the ible Fig. more Early enamel region white spot lesion, in a deciduous molar. The 3.20 Early cavitation in enamel caries. The surface layer of the white Fig. Early cavitationprism cores or interprismatic substance. (By kind permission of Dr Kis much larger spot lesion has broken down, allowing plaque bacteria into the enamel. lesion forms below the contact point and in consequence Little.) ue. White spot than an interproximal lesion in a permanent tooth (see Fig. 3.19). lesion (fig.3)

Site of Attack• Cemental or root caries: Root surface is exposed in the oral cavity because of periodontal disease• Recurrent caries: This occur around the margins or at the base of a previously existing restoration.

Rate of Attack• Rampant caries: Rapidly progressing caries involving many or all of the erupted teeth (fig.4)

of strains of the S. mutans group which are able to form cari-ogenic plaque. S. mutans strains are a major component of plaque in human Bacterial polysaccharidesmouths, particularly in persons with a high dietary sucrose The ability of S. mutans to initiate smintake and high caries activity (Fig. 3.2). S. mutans isolated form large amounts of adherent plaquefrom such mouths are virulently cariogenic when introduced to polymerise sucrose into high-molinto the mouths of animals. like, extracellular polysaccharides (gl However, simple clinical observation of the sites (intersti- cariogenicity of S. mutans depends astially and in pits and fissures) where dental caries is active, form large amounts of insoluble extrac ability to produce acid. Box 3.2 Essential properties of cariogenic b • Acidogenic • Able to produce a pH low enough (usual tooth substance • Able to survive and continue to produce • Possess attachment mechanisms for firm tooth surfaces • Able to produce adhesive, insoluble plaq (glucans) Glucans enable streptococci to adhe to the tooth surface, probably via spe way, S. mutans and its glucans may initFig. 3.2 Extensive caries of decidous incisors and canines. This pattern of the teeth and enable critical masses ofcaries is particularly associated with the use of sweetened dummies and Rampant cariessweetened infant drinks. Production of sticky, insoluble, extrace by strains of S. mutans is strongly relate The importance of sucrose in this a high energy of its glucose–fructose bon (fig.4) thesis of polysaccharides by glucosylt other source of energy. Sucrose is thus such polysaccharides. Other sugars are less cariogenic (in the absence of pre

Rate of Attack • Slowly progressive or chronic caries:1. Progressive slowly and involve the pulp2. Most common in adults

Rate of Attack• Arrested caries:Caries of enamel and dentine, including root caries.

Enamel Caries• The pathological features are essentially similar in both sites.• Enamel caries progression is a slow process.• Beginning of enamel caries , microscopically four zones are seen (fig.6)

Zones of Enamel Caries1. Translucent Zone2. Dark Zone3. Body of Lesion4. Surface Zone

Dentin Enamel 1 2 3 41: Translucent Zone2: Dark Zone3: Body of the lesion (fig.6)4: Surface Zone

Translucent Zone• Earliest and deepest demineralization.• More pores than normal enamel.• Pores are more larger, approximately to the size of water molecule.• There is a fall in magnesium and carbonate mineral ions (1% mineral loss)

Dark Zone• 2-4% mineral loss• Some of pores are larger, but other are smaller than those in translucent zone.• Reminrelization has occurred due to reprecipitation of minerals lost from translucent zone.

Body of the lesion• 5-25% mineral loss• Apatite crystal are more larger than in normal enamel• 5% demineralization shows that the area of radiolucency corresponds closely with the size and shape of the body

Surface Zone• 1% mineral loss, about 40um thick• Little change in early lesion• The surface of normal enamel differs in composition from the deeper layer , being more highly mineralized so interpretation of possible chemical changes in this zone is difficult.

Body 5–25% mineral loss Body 5–25% mineral loss Broader in progressing caries, replaced by a broa Broader in progressing car dark zone in arrested ordark zone in arrested or re remineralised lesions Interproximal caries viewed under Surface zone Surface zone loss. A zone of remineralisation resultingremineralisation resulting constant width, a little thicker in width, a 1% mineral 1% mineral loss. A zone of from the diffusion barrier frommineral content of plaque. Relatively Relatively constant and the diffusion barrier and mineral content of plaque. remineralising lesions remineralising le arrested or arrested or polarized light11 Early enamel caries, a white spot lesion, in a deciduous molar. The loss of this layer, allowingloss of this layer, allowing bacteria Cavitation is Cavitation is bacteriaorms below the contact point and in consequence is much larger lesion to enter the to enter the lesion interproximal lesion in a permanent tooth (see Fig. 3.19).12 Early interproximal caries. Ground section in Fig. 3.13 Early interproximal caries. Ground section viewed by polarisedsame lesion 3.14 3.12 and 3.13) viewed dry under3.1 water viewed by Fig. 3.14 The Fig. The same lesion (Figs 3.12 and (Figsto show the full extent of demineralisa po Fig. 3.13 Early intact surfaceafter immersion in quinoline. Quinoline has ised light d light. The body of the lesion and the interproximal caries. Ground section viewed by polarisedfilled theised light to show the full extent of demineralisation. (Figs 3.12–3.14 b Water Quinoline Dry light layer are larger pores, kind permission of Professor Leon Silverstone aThe translucent and dark zones immersion in quinoline. Quinoline hasnelled thein the body of the lesion to disappear (Fig.of Professor Leon Silverstone and the Editor of Dental light after are not seen until the sectionof the fi fi detail larger pores, causing most is kind permission 49 causing most of the fine detail inbut the dark zonelesionits smaller pores is accentuated. Update 1989;10:262.)immersed in quinoline. 3.12), the body of the with to disappear (Fig. Update 1989;10:262.) 3.12), but the dark zone with its smaller pores is accentuated. The dark zone is fractionally superficial to the translucent of new porosities but possibly also to (fig.7) The dark zone is fractionally superficial to the translucent of new porosities but possibly also to remineralisation of zone. Polarised light microscopy shows that the volume of the large pores of the translucent zone so th

Cavity Formation• Once bacteria have penetrated enamel, they reach amelodentinal junction (ADJ) and spread laterally to undermine the enamel• This has 3 major effects

Cavity Formation1. Enamel losses support of dentin thus becoming weak2. Enamel is attacked from beneath3. Spread along ADJ, allows them to attack dentin over wide area (fig.8)

• There is alternating demineralisation and remineralisation, but demineralisation is predominant as cavity formation progresses • Bacteria cannot invade enamel until demineralisation provides pathways large enough for them to enter (cavitation) DENTINE ENAMEL A Bnphotomicrograph of chalky enamel acid. The crystallites of calcium saltshile the prism cores and some of the estroyed. The same appearance is y caries. (By kind permission of (fig.8) Fig. 3.19 Diagram summarising the main features of the precavitation phase of enamel caries as indicated here in this final stage of acid attack Main features of the precavitation phase of enamel caries. The area on enamel before bacterial invasion, decalcification of dentine has begun. The area (A) would be radiolucent in a bite-wing film but the area (B) could (A) would be radiolucent in a bite-wing film but the area (B) could be be visualised only in a section by polarised light microscopy or microradi- ography. Clinically, the enamel would appear solid and intact but the sur- visualized only in a section by polarised light microscopy or face would be marked by an opaque white spot over the area (A) as seen in Figure 3.11 (From McCracken AW, Cawson RA 1983 Clinical and oral microradiography. microbiology. McGraw-Hill.)

Interproximal caries on radiographs (fig.9)

HARD TISSUE PATHOLOGYCHAPTER 3 Fig. 3.24 This marises the seq enamel from th lesion to early c relates the diffe development o Sequential changes in enamel from the stage of the radiographic ap initial lesion to early cavity formation clinical findings lent by the late and reproduced Editor of the Br (fig.10) 1959; 107:27–

Caries in Dentin• Caries of the dentine develops from enamel caries; when the lesion reaches the amelodentinal junction.• The caries process in dentine is approximately twice as rapid in enamel.

Zone of Dentin Caries• Zone of Sclerosis• Zone of Demineralization• Zone of Bacterial invasion• Zone of Destruction

Zone of Sclerosis• The sclerotic or translucent zone is located beneath and at the sides of the carious lesion.• Dead tract may be seen running through the zone of sclerosis because the death of odontoblast at an earlier stage in the process of caries.

Zone of Demineralization• In the demineralization zone the intratubular matrix is mainly affected by a wave of acid produced by bacteria in the zone of bacterial zone.• It may be stained yellowish –brown as a result of the diffusion of other bacterial products interacting with proteins in dentine.

Zone of Bacterial Invasion• In this zone bacteria extend down and multiply within the dentinal tubules• The bacterial invasion probably occurs in two waves: i. 1st wave consist of acidogenic organism, mainly lactobacilli , produce acid which diffuses ahead into the deminrelized zone. ii. 2nd wave of mixed acidogenic and proteolytic organism then attack the diminrelized matrix.

Zone of Bacterial Invasion• In addition thickening of the dentinal tubule due to the packing of the tubules by microorganism.• Tiny “liquefaction foci” are formed by the break down of the dentinal tubule.• This focus is an ovoid area of destruction , parallel to the course of the tubule and filled with necrotic debris.

Zone of Destruction• In th is zone of d e s t r u c t i o n , t h e liquefaction foci enlarge and increase in number.• T h i s p ro d u c e s c o m p re s s i o n a n d distortion of adjacent dentinal tubules.

Reactionary Changes in Dentin• Tubular Sclerosis• Regular Reactionary Dentin• Irregular Reactionary Dentin• Dead Tracts

Reactionary Changes in DentinThe carious involvement of secondarydentine does not differ remarkably fromthe involvement of the primary dentine ,except that is usually somewhat slowerbecause the dentinal tubule are fewer innumber and more irregular in their course ,thus delaying penetration of the invadingmicroorganism.

Reactionary & Tertiary Dentin• Eventually however the involvement of the pulp results with ensuing inflammation and necrosis.

Root surface caries• Develops on exposed root surfaces due to gingival recession• Forms stagnation areas for plaque• Cementum is readily decalcified

Root surface caries• Cementum softens beneath the accumulated plaque over a wide area• Saucers shape cavity• invaded along the direction of Sharpey’s fibers

Root surface caries (fig.10)

Root surface caries• Spread between lamellae along the incremental lines• Dentin becomes split up & progressively destroyed by combination of demineralization and proteolysis

Arrested Caries & RemineralizationUnder favorable conditions, cariousdemineralization can be reversed1. Fluoride application2. consumption of less cariogenic diet

Arrested Caries & Remineralization• white spot may become arrested• adjacent teeth is removed resulting in removal of stagnation area• remineralized by minerals from enamel

Arrested Caries & Remineralization• Dentin caries may be occasionally be arrested as a result of extensive destruction of enamel resulting in wider area of dentin becoming involved

References• J. V. Soames, J. C. Southam, “Dental Caries” in Oral Pathology, 4th Edition, Oxford University Press, 2007 pp 19-31.• R. A. Cawson, E. W. Odell, “Dental Caries” in Cawson’s Essential of Oral Pathology and Oral Medicine, Eighth Edition, Churchill Livingstone Elsevier, 2008 pp 40-59.

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