Unit 21. Microbiology of caries 23_24.pdf

Microbiology Unit 21 Microbiology of caries Ve más allá 1 DENTAL CARIES DEFINITION:  Chronic infectious disease that results in the destruction of tooth tissues as a result of the acid produced by certain bacteria in dental plaque.  Cavities can affect: enamel, dentin and cement Relevance o...

Microbiology Unit 21 Microbiology of caries Ve más allá 1 DENTAL CARIES DEFINITION:  Chronic infectious disease that results in the destruction of tooth tissues as a result of the acid produced by certain bacteria in dental plaque.  Cavities can affect: enamel, dentin and cement Relevance of dental caries • It is not a serious illness but: • It is one of the most common diseases in humans • Important economic costs and time-consuming • Produces pain that can be severe • It can produce functional consequences (chewing problems ...) • Aesthetic consequences • It can be the source of infection in neighboring and distant tissues (endocarditis) Epidemiological importance of caries  Caries is one of the most frequent infections in modern societies: in Spain it affects 40% of the population.  Spain is one of the European countries with the highest levels of cavities, surpassing Germany, France, Switzerland, Holland and the United States. Classification Dental caries can be classified according to the location of the lession: a) Pit or fissure caries b) Smooth surface caries c) Root surface caries d) Interproximal surfaces caries Recurrent caries: associated with an existing restoration. Theories of dental caries  Legend of the worm: VII century BC  Endogenous theories (greeks): diseases are due to imbalances in humors (blood, bile ...)  Exogenous theories (early XIX):  Acidogenic theory  Parasitary theory: by microorganisms Theories of dental caries  Chemoparasitic theory of Miller (late 19th century): cavities are due to the acids produced by microorganisms from sugars. The concept of bacterial plaque was not known nor was it known which microorganisms were cariogenic.  Proteolytic theory (mid 20th century): Proteolytic enzymes produced by bacteria cause tooth decay.  Theory of proteolysis-chelation (mid-20th century): bacterial proteolytic enzymes degrade organic matter releasing chelating agents that dissolve tooth minerals. CURRENT aetiological theory (since 1961) KEYES SCHEME Three factors involved: • Tooth: is what is destroyed (target) and its resistance is variable (composition, fluoride, saliva) • Substrate (diet): (carbohydrates) nutrients for bacteria • Oral microbiota: acid-producing bacteria Multifactorial disease Necessary interaction of the 3 factors for a sufficient time 1.-TOOTH: a) Anatomical features: pit and fissure caries of the occlusal surface (retention). b) Age: the tooth is more sensitive among individuals aged 3 or 4 years, after eruption (when enamel maturation is reached). c) Fluoride: systemic or topical, it makes the enamel more resistant to acid d) Altered arrangement of teeth and malocclusion e) Braces (orthodontic appliances) f) Saliva (self-cleaning, buffer pH, remineralization, antimicrobial factors). Problems in patients with xerostomy or hyposalivation. 2.-FOOD • Association between sugar consumption and caries. • The most cariogenic sugar is sucrose • The cariogenic power of food depends on:  Quantity of sugar consumed  Type of sugar  Consumption frequency  Adhesion of food to the teeth (gummy candy, honey, nuts & sugar ...) 3.- MICROBIOTA A. Streptococcus mutans B. Lactobacillus spp C. Actynomyces spp A. Streptococcus mutans • Before the introduction (5 centuries ago) of sucrose in food, dental caries were rare and only occurred in adults. • The introduction of sucrose changed oral ecology, giving S. mutans a huge advantage. • Children are colonized by S. mutans between 19 and 31 months of age from their cohabitants. • 24% of colonized children under 3 years present an average of 3 - 4 carious lesions, while those not colonized are free of caries. • There is a statistically significant correlation between counts of S. mutans in saliva and caries prevalence. 1. Cariogenicity factors of S. mutans • Produce insoluble extracellular polysaccharides from sucrose that help them to adhere to tooth surfaces and bind more bacteria (dental plaque). • Soluble extracellular polysaccharides are produced and used as nutrients • Accumulate large amounts of glycogen, so that when sucrose is depleted in the environment they can continue producing lactic acid. • It is an acidogenic bacteria. From sucrose they produce large amounts of organic acids • Acidophilic, aciduric Streptococcus mutans Acidogenic Acidophilic Aciduric Acid production Grows at acid pH Acidifies acidic pH 2.- Cariogenicity factors of Lactobacillus spp: • Acidogenic (produce large amounts of acid), acidophilic and aciduric. • They have a low ability to colonize the tooth surface. Therefore unimportant at the beginning of the lesion of tooth surfaces • Very low proteolytic activity • Very important in the progression and dentin lesions. 3.- Cariogenicity factors of Actinomyces spp: • A. viscosus predominates • Acidogenic • Some produce extra and intracellular polysaccharides (used mainly as nutrients). • They have fimbriae: colonization • They have proteolytic activity (dentine caries) PATHOGENESIS OF DENTAL CARIES • Acid produced by cariogenic bacteria decreases the pH in the oral environment • When the pH drops below 5.3 to 5.7 (pH critical) demineralization of enamel starts (hydroxyapatite is dissolved) • Frequent glucidic contributions determine long acid periods. These conditions favor aciduric bacteria (S. mutans and lactobacilli) that become the predominant bacteria PATHOGENESIS OF DENTAL CARIES • When the pH increases, calcium phosphate returns to enamel: remineralization. • If the demineralization and remineralization process are in balance, the integrity of the tooth surface is maintained. • If the balance is broken in demineralization, caries appears. favor of M I N E R A L I Z A T I O N pH 5.3-5.7 D E M I N E R A L I Z A T I O N **origen of alkalis: • Saliva • Amonia production by proteolytic bacteria • Protein intake acids* *origen of acids: • Acidogenic bacteria (fermenting sugars) • Intake of sugars and acids alkalis** PATHOGENESIS OF DENTAL CARIES The balance can be broken in three ways: • Excessive production of acids • Decreased protective power of saliva (hyposialia, asialia, Sjögren's syndrome) • Repeated and frequent intake of fermentable sugars. PATHOPHYSIOLOGY OF CARIES 1-THE BEGINNING OF THE PROCESS • Enamel caries • Root caries 2-DEVELOPMENT PROCESS • Caries of dentine PATHOPHYSIOLOGY OF CARIES 1-THE BEGINNING OF THE PROCESS 1.1 Enamel Caries: Dental caries initially affects the crown (enamel covered completely) so the initial lesion of caries (white spot) usually affects the enamel. a.-Pit and fissure decay: they are the most frequent. S. mutans and Lactobacillus predominate PATHOPHYSIOLOGY OF CARIES b.-Aproximal surface caries: next in frequency Actinomyces, Streptococcus mutans and Lactobacillus predominate c.-Smooth surface caries: are rare Streptococcus mutans predominate PATHOPHYSIOLOGY OF CARIES 1.2 Root Caries: it can begin when the root is exposed by gingival recession. The cement has a higher proportion of organic matter than enamel so as well acidogenic bacteria and proteolytic bacteria can also be involved. Actynomices spp will predominate. PATHOPHYSIOLOGY OF CARIES 2.-DEVELOPMENT PROCESS: Caries of dentin: When the bacteria reach the dentin there is a different environment: • Anaerobic conditions • Higher content of organic substrates which favors the development of proteolytic bacteria. Lactobacillus predominate There are usually anaerobes and no Streptococcus mutans. If the lesion advance: pulpitis. -Streptococcus mutans : predominate on the enamel (smooth surfaces, pits and fissures and aproximal surfaces) - Actinomyces and Lactobacillus : predominate in tissues (root, dentine) Streptococcus dentisani • Isolated from the oral cavity of people without caries • Inhibition of S. mutans growth: bacteriocins • Buffer capacity López-López A, Camelo-Castillo A, Ferrer MD, Simon-Soro Á, Mira A. Health-Associated Niche Inhabitants as Oral Probiotics: The Case of Streptococcus dentisani. Frontiers in Microbiology 2017;8. CONTROL OF FACTORS RELATED WITH DENTAL CARIES 1. Control of dietary habits 2. Fluoride 3. Pit and fissure sealants 4. Control of dental plaque CONTROL OF FACTORS RELATED WITH DENTAL CARIES 1.-CONTROL DIETARY HABITS a) Rationalize the consumption of sugars (in quantity and frequency) b) Decrease consumption of adherent foods c) Replace sucrose with: • Sugars such as glucose, fructose, invert sugar (glucose + fructose). They are less cariogenic than sucrose but can be metabolized by streptococci • Lactose is better but not very sweet CONTROL OF FACTORS RELATED WITH DENTAL CARIES • Polyols (sugar alcohol derivatives of): • Mannitol and sorbitol:  They can cause osmotic diarrhea  Streptococcus mutans metabolize them but slowly • Xylitol:  Sweeter than mannitol and sorbitol  Cause diarrhea  It is not cariogenic  Antimicrobial effect  It is more expensive CONTROL OF FACTORS RELATED WITH DENTAL CARIES • Noncaloric sweeteners: • They are very sweet and have few calories • They are not metabolized by bacteria so they are not cariogenic. • Saccharin, cyclamate and aspartame. CONTROL OF FACTORS RELATED WITH DENTAL CARIES 2.-Fluoride Systemic-fluoride: -In water -In milk, salt, tablets ... Topic-fluoride: Toothpastes, gels, varnishes, mouthrinses Excessive fluoride: mottled enamel or dental fluorosis CONTROL OF FACTORS RELATED WITH DENTAL CARIES Fluoride. Mechanisms for prevention of dental caries: • Fluoride replaces hydroxyl groups of hydroxyapatite to form fluorapatite which is more resistant to acid effects. • Facilitates the remineralization of initial caries lesions (white spot). • Inhibits bacterial metabolism. CONTROL OF FACTORS RELATED WITH DENTAL CARIES CONTROL OF BACTERIAL PLAQUE Mechanical removal of plaque (brushed..) Antiseptics (in mouthwashes, gels ..) Identifying patients at high risk of caries Vaccine against cavities? IDENTIFICATION OF PATIENTS WITH HIGH RISK OF DENTAL CARIES • Patient history (diet, age, oral hygiene ..) • Exploration (level of hygiene, restorations, incipient caries, braces ...) • MICROBIOLOGICAL TESTING:  Lactobacillus load in saliva (DentoCult)  Streptococcus mutans load in saliva (DentoCult):Colony forming units (CFU) per milliliter of saliva  Tests for acid production capacity: Snyder and Alban test THANKS FOR YOUR KIND ATTENTION! QUESTIONS PLEASE? Ve más allá © Copyright Universidad Europea. Todos los derechos reservados