Dental Caries Zahraa - Part 1 PDF

Dental caries Dr. Al-zahraa Mohamed El-marhomy Restorative Dentistry Department Faculty of Dentistry- Tanta university  Intended Learning outcomes (ILOs) a2. Describe concept of cariology. a3. Define different classifications of carious lesions. a4. Determine the management of car...

Dental caries Dr. Al-zahraa Mohamed El-marhomy Restorative Dentistry Department Faculty of Dentistry- Tanta university  Intended Learning outcomes (ILOs) a2. Describe concept of cariology. a3. Define different classifications of carious lesions. a4. Determine the management of carious lesions. Contents: Introduction Definition Etiology Pathogenesis of D.C. Histopathologic features Classification Clinical signs & symptoms Diagnosis of D.C. Prevention of D.C. Management of D.C. Introduction ▪ Dental caries is commonly known as tooth decay. ▪ In the minds of the lay person, and surprisingly even within dentistry, dental caries is often thought of as holes in the teeth rather than an entire disease process. ▪ Dental caries is one of the most prevalent chronic diseases of people worldwide; individuals are susceptible to this disease throughout their lifetime. ▪ One of the most major causes of tooth loss and oral pain. Definition ▪ also known as “ tooth decay or a cavity”. ▪ a complex, multifactorial, biofilm dependent disease, bacterial in origin, that causes demineralization and destruction of the hard tissues of the teeth (enamel, dentin and cementum) followed by destruction of the organic substance of the tooth structures. It has now been proven that caries is “a dynamic disease” having intermittent phases of demineralization by organic acids of microbial origin followed by remineralization by salivary components (or therapeutic agents). A non-cavitated carious lesion are characterized by mineral loss beneath an apparently intact enamel surface layer creating porosities that change the refractive index of the normally translucent enamel typically characterized by white or opaque areas on enamel surfaces, thus called “white spot lesions”. Etiology ▪ Etiology of dental caries is generally agreed to be a complex problem complicated by many indirect factors that obscure the direct cause or causes. ▪ No universally accepted opinion. ▪ No single theory old or new can justify all aspect of caries.  the acidogenic theory  the proteolytic theory  proteolytic-chelation theory ▪ Proposed by Miller in 1884. ▪ Stated that dental decay is a chemo-parasitic process. ▪ it states that caries is caused by acids produced by microorganisms of the mouth. ▪ Acid derived from the fermentation of carbohydrate lodged in the retaining centers of the teeth. ▪ He assigned an essential role to three factors in the caries process: 1. The oral microorganism. 2. The carbohydrate substrate. 3. The acids. ▪ Two stages : 1. Decalcification of enamel, which results in destruction & decalcification of dentin. 2. dissolution of softened residue ▪ Draw backs in theory: ✓ Predilection of certain specific sites on a tooth ✓ why some populations are caries free ? ✓ Doesn't explain phenomenon of arrested caries theory ✓ Implicates the study of role of carbohydrates, microorganisms, acids and dental plaque ▪ Proposed by Gottlieve in 1944. ▪ Caries is essentially proteolytic process. ▪ This theory proposed that the organic & protein elements were the initial pathway of invasion by micro-organisms. Proteolytic micro-organisms invade the organic component of the tooth Liberation of Proteolytic enzymes Destruction and dissolution of the organic matrix of the tooth Formation of acids “Amino Acids” Demineralized of the inorganic part of tooth ▪ Proposed by Schatz in 1955. ▪ Simultaneous microbial degradation of organic components (proteolysis) & dissolution of inorganic components of tooth by process called (chelation). ▪ The word “chelate” refers to compound that can bind metallic ions such as calcium, iron, copper, zinc etc. by valence bond. ▪ It considers dental caries to be a bacterial destruction of teeth where the initial attack is essentially on the organic components of enamel. ▪ The breakdown products of this organic matter have chelating properties and thereby dissolve the minerals in enamel Caries occurs when there is interaction of 3 principal factors: 1. The Host. 2.The Micro flora. 3.The Substrate. (diet) a. Tooth ✓ physical factors (quality of diet) ✓ composition ✓ local factors carbohydrate, vitamin ✓ morphologic characteristics and fluorine content ✓ position b. Saliva ✓ composition ✓ PH ✓ quantity ✓ viscosity ✓ antibacterial factors  A. Tooth: ▪ Morphology and position: ✓ Deep pits & fissures make tooth susceptible to caries because of food impaction & bacterial stagnation. ✓ Irregularities in the arch form , CROWDING & OVERLAPPING also favor the development of caries. ✓ Partially impacted third molars are more prone to caries. ✓ First molar is the most susceptible tooth in the dental arch. ✓ Maxillary teeth are more susceptible than mandibular teeth.  A. Tooth: ▪ Chemical nature: ✓ The surface of enamel has more minerals & organic matter & relatively less water. ✓ In addition, certain elements like fluoride , chloride , zinc , lead accumulate more on the surface enamel than the sub surface enamel. ✓ With passage of time teeth become more resistant to caries because of decrease in permeability. B. Saliva: ▪ Quantity: ✓ The quantity has definite influence on caries. ✓ Human beings suffering from decreased flow of saliva or lack of salivary secretions usually showed high rate of dental caries. ✓ Certain drugs influence salivary flow & in turn results in caries. Drugs which lead to xerostomia include anti depressant, antihistamines etc. ▪ Viscosity: ✓ Viscous, ruby saliva reflects less water content and thus affects the oral clearance rate. ▪ B. Saliva: ▪ Composition: ✓ The composition of saliva varies considerably. ✓ Caries prone individuals have low calcium & Po4 phosphorus levels. ✓ The caries immune persons exhibit a greater Amonnia content in saliva which retards the plaque formation & neutralizes acid formation to a certain extent. ✓ Fluoride enhances rate of remineralization of enamel, formation of a fluorhydroxyapatite which increases resistance of enamel to acid attack. F ▪ B. Saliva: ▪ PH of saliva: ✓ The normal PH of saliva is 6-7. ✓ a fall in PH of saliva, decrease buffering capacity of saliva leads to increase in caries incidence. ✓ The PH at which any saliva ceases to be saturated with calcium & phosphorus is referred to as critical PH (5.5) ▪ B. Saliva: ▪ Antibacterial properties: ✓ Lysozyme: an antibacterial agent present in saliva – can inhibit micro-organism in oral cavity to some extent, but its role in caries inhibition is doubtful. ✓ Antibodies: like IgA & IgG against specific bacteria have been reported in human saliva. 2. The microflora ▪ Major organisms responsible for caries are:- Strep mutans ,Lactobacilli and Actinomyces. ▪ These different organisms display some selectivity as to which tooth surface they would prefer. ▪ Streptococcus mutans plays a vital role in initiation of caries. (d.t. their ability to adhere to tooth surface) ▪ the streptococcus mutans: ✓ Produces lactic acid from sucrose ✓ Can live at PH as low as 4.2 (more aciduric than other streptococci). ✓ Forms large amounts of extracellular, sticky, insoluble glucan plaque matrix. ✓ Adheres to pellicle and contributes to plaque formation. ▪ In Deep dentinal caries predominantly, present micro- organism are lactobacilli which account 1/3rd of the oral flora. ▪ Require retentive areas to proliferate and hence a high count is usually associated with the presence of the frank cavitation. ▪ Acidogenic and aciduric. ▪ The organism involved in root caries (cemental caries) are different from those in smooth surface lesions Predominantly Actinomyces viscosus have been isolated.  Diet is the third factor in initiation & progression of caries. ▪ Physical nature of the diet: ✓ The intake of refined carbohydrate is corelative with the concentration of acid producing bacteria and dental caries. ✓ Fibrous and tough food should be eaten at the end of the meal to naturally scrub the teeth and gingival tissue during mastication. ▪ Chemical nature of the diet: ▪ The carbohydrate content of diet has been almost universally accepted as one of the most important factors in dental caries process. ▪ Only refined carbohydrates are effective. ▪ For caries production following factors are responsible : a)Type of carbohydrate e.g., monosaccharide's, disaccharides or polysaccharides. b) Frequency of intake. c) Time of stagnation. ▪ Chemical nature of the diet: ▪ Sucrose is unique in that it can serve in the formation of insoluble extracellular polysaccharides & thereby enhance plaque formation & microbial aggregation on the tooth surface. ▪ Another factor promoting caries is the consumption of snacks between meals. ▪ Vitamin's content of the diet: ▪ Vit D and Vit K appear to have some role in the caries process. ▪ Vit D may have an indirect effect on caries process. Its deficiency can cause enamel hypoplasia which can make the tooth more susceptible to caries. ▪ Vit K has enzyme inhibiting action in carbohydrate degradation cycle. Can be utilized as an anticariogenic agent. ▪ Calcium and phosphorous content: ▪ Florine content: ▪ Topical and water fluoridation has been known to be effective in caries control, dietary fluorine may have no role. ▪ Time is another significant factor in the development of dental caries. ▪ Earlier it was a key's traid consisting of host , microflora & substrate , later time factor was added. ▪ During long intervals of undisturbed plaque stagnation , the plaque PH is lowered favoring the production of organic acids that demineralize tooth structure. Traditionally, all the factors have to be present at the same time with the same intensity to produce the disease. Recently, It is indeed true that multiple factors have to act in concert with each other to produce the disease, but not necessarily at the same time. To explain this inadequacy, the circles are simply rearranged in a different manner and the factors have been categorized as ‘determinants’ and ‘confounders’ ❖ Determinants: o is anything that determines the outcome. o Most of the major and minor components are determinants because of the way(s) they interact with each other to determine the outcome — enamel dissolution. Pathogenesis of D.C.  Enamel pellicle + Bacteria 1 Plaque formation 2 Plaque bacteria + Fermentable carbohydrates 3 4 Acid production 5 Acid + Enamel Demineralization and dissolution of inorganic 6 and organic structures of tooth 7 Dental caries ▪ It is also known as “DENTAL BIOFILM, MICROBIAL PLAQUE”. ▪ Dental plaque is a biofilm or mass of bacteria that grows on surfaces within the mouth. ▪ In order to persist, oral micro-organisms have to attach to a surface & grow; otherwise, they will be lost from habitat. ▪ BIOFILM-consists of bacteria (90%) and its byproducts and extracellular polysaccharide matrices. ▪ ORAL BIOFILM is a structure of vital significance as contributing factor to the initiation of dental caries.  1. Pellicle formation 2. Microbial colonization 3. Microbial succession 4. Mature biofilm 1. Pellicle formation: ▪ Micro-organisms do not colonize directly on the mineralized tooth surface. ▪ The teeth are always covered by an acellular proteinaceous film; this is the pellicle that forms on the ‘naked’ tooth surface within minutes to hours.  1. Pellicle formation 2. Microbial colonization 3. Microbial succession 4. Mature biofilm 2. Microbial colonization: ▪ As the microbial cell approaches the pellicle-coated surface, long-range but relatively weak physicochemical forces between the two surfaces are generated & these forces may facilitate the attachment. ▪ Colonization occurs in 4-24 hrs. after the pellicle formation.  1. Pellicle formation 2. Microbial colonization 3. Microbial succession 4. Mature biofilm 3. Microbial succession: ▪ the initial establishment of a streptococcal flora appears to be a necessary precursor for the subsequent proliferation of other organisms.  1. Pellicle formation 2. Microbial colonization 3. Microbial succession 4. Mature biofilm 4. Mature biofilm: ▪ After about a week of undisturbed growth, the microflora develops into a climax community that harbors a broad range of bacterial species. ▪ plaque bacteria can form acid from sugars over long periods to attack tooth surfaces. ▪ Production of high acid concentration contributes to low ph. To explain the role of dental biofilm in the etiology of dental caries…!!! ❑The Non-specific Plaque Hypothesis: which considered that disease is the outcome of the overall activity of the total plaque microflora, which is comprised of many bacterial species. ❑The Specific Plaque Hypothesis: which proposed that only a few specific species, such as “Streptococcus mutans” are actively involved in the disease. ❑ This hypothesis focused efforts on controlling disease by targeting preventive measures & treatment against a limited no. of organisms, such as by vaccination or gene therapy or by antimicrobial treatment. The ecological plaque hypothesis: ▪ Reconciles key elements of the earlier two hypothesis. ▪ Proposes that the organisms associated with disease may also be present at sound site , but at too low level. ▪ Disease is a result of a shift in the balance of the resident microflora driven by a change in local environmental conditions. ▪ Sturdevant’s art & science of operative dentistry 5th edition pg no. 288- 289 ▪ SHAFER’S TEXTBOOK OF ORAL PATHOLOGY 5th edition PG NO. 590 – 597 ▪ DENTAL CARIES the disease & its clinical management 2nd edition ; OLE FEJERSKOV & EDWINA KIDD pg.no. 168-169 ▪ Clinical Operative Dentistry- Principles & Practice : RAMYA RAGHU pg no. 76 ▪ Essential Of Public Health Dentistry – Soben Peter 5th edition pg no. 528 ▪ Selwitz RH, Ismail AI, Pitts NB. Dental caries. The Lancet. 2007;369:51-59. ▪ Pitts NB, Zero DT, Marsh PD, et al. Dental caries. Nat Rev Dis Primers 2017;3(1):17030 ▪ Sonis ST. Dental Secrets. 3rd edition. Philadelphia. 2003; pp130. ▪ Sonis ST. Dental Secrets. 3rd edition. Philadelphia. 2003; pp130. ▪ Fejerskov O and Kidd E. Dental caries: the disease and its clinical management. 2nd edition. Blackwell Munksgaard, Copenhagen, 2008; pp 356-360. ▪ Pitts NB, Zero DT, Marsh PD, Ekstrand K, Weintraub JA, Ramos-Gomez F, Tagami J, Twetman S, Tsakos G, Ismail A. Dental caries. Nat Rev Dis Primers. 2017 May 25;3:17030., dr. Robert L Selwitz Volume 369, No. 9555, p51–59, 6 January 2007) ▪ Pitts NB, Twetman S, Fisher J, Marsh PD. Understanding dental caries as a non-communicable disease. Br Dent J. 2021 Dec;231(12):749-753. ▪ Ghodasra R, Patel R, Brizuela M. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Mar 9, 2022. Dental Caries Diagnostic Testing. ▪ Schwendicke F, Dörfer CE, Schlattmann P, Foster Page L, Thomson WM, Paris S. Socioeconomic inequality and caries: a systematic review and meta-analysis. J Dent Res. 2015 Jan;94(1):10-8. Dr.Zahraa M.