Topic+54+- Defense Mechanism of the Oral Cavity- Caries & Pulpitis_2024.pdf

MOSDOH 5303 Defense Mechanism of the Oral Cavity Caries & Pulpitis...

MOSDOH 5303 Defense Mechanism of the Oral Cavity Caries & Pulpitis Fall 2024 Topic 54 Priscilla Phillips, PhD Copyright © 2024, A.T. Still University/Missouri School of Dentistry & Oral Health. This presentation is intended for ATSU/Missouri School of Dentistry & Oral Health use only. No part of this presentation may be distributed, reproduced or uploaded/posted on any Internet web sites. Copyright Disclaimer : Certain figures/tables are included under the fair use exemption of the U.S. Copyright Law and have been prepared according to the educational multimedia fair use guidelines and are restricted from further use.  1. The features of the oral cavity that act as barriers to infection and common risk factors that may Defense compromise these barriers Mechanisms 2. The mechanisms microorganisms have to penetrate these barriers monocyte phagocytosis Neutrophil phagocytosis Secretory IgA  Natural Barriers to Oral Tissue Infection Natural barriers that inhibit microbial penetration include ◆ Tissue integrity ◆ Host immunity ◆ Oral secretory fluid production Each barrier to oral infection is impacted by whole human health Hard (teeth) and soft tissue (mucosa) integrity and function, affected by overall host health, include: ◆ Congenital (e.g., genetic) and Systemic (e.g., age, pregnancy) factors that modify the host immune response, connective tissue development, bone development, or metabolism, leading to observed oral tissue integrity and function. ◆ These factors inherently define an individual’s susceptibility to infectious disease and degree of pathology Alterable risk factors (e.g., behavioral, environmental) for development of infectious disease that impact oral tissue integrity: 1. Oral Hygiene –MOST IMPORTANT 2. Toxins or Biocides –dramatically affect local environment and microbial ecology in the oral cavity (antibiotics) and / or host immune response (smoking, radiation) 3. Diet – Composition (high sugar diet), consistency (sticky, low solubility), and frequency of intake (feast – famine cycle) 4. Medication – such as those that cause dry mouth or impact vascular function 5. Mechanical abrasive forces – Such as Receding gums from Cementum and Bruxism: Teeth grinding brushing too hard dentin is more vulnerable to microbial invasion than enamel Oral Mucosa Function: Protection, sensation, secretion ** Natural barriers of the oral mucosa to microbial tissue infection (i.e., inhibit microbial penetration) Highly vascularized ◆ highest = free gingiva Gingival vasculature Selliseth and Selvig, 1994 Oral Mucosa Function: Protection, sensation, secretion Keratinized areas: Areas typically subject to abrasion 1. Gingiva (~90%), Keratinized 2. Roof of the mouth (hard palate) gingival epithelium 3. Dorsum (top) of the tongue and Sulcus papillae 4. Vermillion border of the lip (a keratinization transition zone) Gingiva Alveolar Bone Oral Mucosa Function: Protection, sensation, secretion Non-keratinized areas: 1. Sulcular epithelium (lines the sulcus) Site most vulnerable to infection 2. Junctional epithelium 3. Lining mucosa – Epithelium that Sulcus lines the lips, cheeks, floor of Junctional mouth, ventral side of the epithelium tongue, soft palate, and alveolar mucosa, which abuts the scalloped edge of the Gingiva mucogingival junction Alveolar Bone Mucogingival junction Chronic Soft Tissue Infection Mechanisms of microbial persistence at the epithelium ◆ Microorganisms capable of invading host cells may persist for days (e.g., inhibit/redirect/or resist intracellular Lysosomal degradation) e.g, P. gingivalis e.g, S. mutans – tolerate low pH ◆ Bacteria may cycle out to re-infect new host cells and disseminate Endocytosis Exocytosis Endosome Surface X receptor Endosome/Lysoso interactions Lysosome me fusion Chronic Soft Tissue Infection Mechanisms of microbial persistence at the epithelium e.g, hide surface antigens using EPS ◆ Surface attached biofilm “Hide”, redirect, or overwhelm the host immune response resulting in collateral damage ◆ Biofilm: increased tolerance to antibiotics and antiseptics Antibodies Immune Biofilm Y Y response secreted molecules Y ROS Y Biofilm Formation EPS Phagocytes matrix TLRs Surface Cytokines receptor interactions  Mechanisms of immune Mucosal Immunity protection at mucosal surfaces Humoral immunity: Soluble & insoluble molecules in lymph/blood Cellular immunity: Tissue and circulating cells such as neutrophils (PMNs), the first cellular line of defense against bacterial infection Neutra et al. Nature Reviews Immunology 6, 148–158 (February 2006)  Oral Lymphatic System: Summary Review ◆ Microbes that have passed Oral Lymphatic Organs ** through oral epithelium may Lymph nodes enter nearby lymphatics Tonsils directly, or be transported to them by phagocytic cells, Itra-oral Lymphoid Tissue ** eliciting an immune response. Palatine and lingual tonsils: B-cells and perifollicular T-cells. Antigens penetrate through covering epithelium (no afferent lymphatics) Salivary gland lymphoid tissue: Concerned mainly with synthesis of secretory IgA Gingival lymphoid tissue: Plasma cells, lymphocytes, macrophages and PMNs. Important in immunological response to dental plaque Scattered submucosal lymphoid cells Oral Secretory Fluid Production Acts as a barrier to oral infection through: 1. Immunological components provided by oral fluids 2. Mechanical forces (e.g., washing, swallowing) determined by oral fluid flow rate Even with strong teeth, good hygiene, and a healthy diet, changes in the ORAL FLUID production, in terms of volume or components, affects overall oral tissue health. xerostomia: mouth breather; Sjogren’s syndrome, etc. Oral Fluids Whole saliva (mixed saliva) contains: 1. Salivary gland secretions (soluble) 2. Gingival Crevicular fluid (soluble and cellular) 3. Factors derived from the host diet or hygiene practices (soluble) ** Soluble Factors in saliva important electrolytes for oral health nutrients waste metabolite most abundant protein  Saliva: Components secreted by the salivary glands 1. Similar to serum Whole ** ∧ 2. Mechanical function Lubrication Clearance (rinse) 3. Primary immunological factor is secretory IgA (some IgG) – continuously secreted, although upregulated with stimulation Secreted through the gingival crevice, not the salivary glands. (See CGF)  Sulcus Enamel Internal Gingival Crevicular Fluid (CGF) basal lamina External basal lamina Secreted by the junctional epithelium Junctional Fluid flow increases with inflammation and epithelium mechanical stimulation. Immunological components of CGF Antibodies: IgM, secretory IgA, IgG, Complement Phagocytes: mainly neutrophils, and some macrophage and lymphocytes Cytokines (e.g., interleukins, TNF), indicative of a disease state (inflammation) Similar to serum (tissue exudate) Other secreted host defense factors (e.g., enzymes, proteinases) increase in response to bacteria  ** Cellular (PMNs) components come from GCF fluid The primary soluble and cellular components in gingival crevicular fluid (GCF), salivary gland secretion and whole (mixed) saliva Question: A true statement about oral fluids secreted by the salivary glands 1. Salivary glands secrete lysozymes that function to cleave the bond between N-acetyl glucosamine and N-acetyl muramic acid in bacterial cell walls 2. Salivary glands only secrete IgA when stimulated by the development of caries or periodontal disease 3. Salivary glands is the primary source of leukocytes that function to protect the oral mucosa  1. Definition, demographics, and subtypes 2. Determinants of dental health 3. Acidogenic theory of caries Dental 4. Caries etiology 5. Streptococcus mutans: A commensal Caries organism, a cariogenic pathogen, and strain dependent associated with extra- oral disease Dental Caries Dental caries is a chronic infection of enamel or dentine. ◆ In the U.S., 1 in 5 people have untreated caries and ~75% have existing dental restorations ◆ More than 125 systemic health conditions are affected by oral health Dental Caries ◆ Most prevalent childhood disease in the U.S. ◆ Disproportionately affects minorities and low-income populations ADA, 2013  Determinants of Dental Health Oral fluid (whole saliva) volume and components Rate of Secretion: Depends on age, sex, time of day, genetic factors Flow: Slow moving thin film (~0.1mm; unstimulated flow rate of 0.8mm/min - 8mm/min) Not uniform: Distinctly different fluid environments depending on the site (oral cavity architecture). Insufficient Saliva is a key host risk factor for caries Xerostomia (dry mouth): Etiology (cause): Genetic, acquired disease (e.g., Sjögren syndrome), diet (e.g., dyhydrated), medication, or behavior (e.g., mouth breather) Outcomes: altered buffering capacity, remineralization capacity, flow, and antimicrobial factor availability  Determinants of Dental Health Enamel integrity: congenital defects and environmentally caused defects (abrasion, acid reflux) are key host risk factor for caries development  Determinants of Dental Health Plaque: bacterial biofilm ◆ Caries do not form without plaque Dental caries is a biofilm disease! Plaque is especially cariogenic when dominated by high acid producing facultative anaerobes!  Determinants of Dental Health Diet: high sugar, especially sucrose, is a major risk factor for caries development ◆ Frequency, rather than total intake (quantity) appears to be the decisive factor, along with stickiness and concentration.  Determinants of Dental Health Time modulates the relative contributions of other risk factors ◆ Sugar retention ◆ Age (host) ◆ Biofilm accumulation/retention (i.e., an uncared-for-mouth)  Acidogenic Theory of Caries Expansion of “The plaque model of disease”, to better define the etiology of enamel erosion (caries), can be summarized as follows: Plaque accumulation in the presence of carbohydrates leads to acid production (microbial metabolic waste), inhibiting remineralization by salivary components and favoring demineralization. The rate of decay depends on host diet (type, availability and frequency), time, and tooth susceptibility. Acidogenic Theory of Caries: Stephan Curve First described in 1943, shows the rapid fall rate of salivary pH below the critical level after consumption of carbohydrates (within a few minutes ~ 5-10 min) a typical quick rise rate (~20-30min) indicative of acid elimination in saliva between periods of consumption. Acidogenic Theory of Caries: Stephan Curve Critical pH 5.5 pH of saliva remains fairly constant between meals because it is buffered by bicarbonate (primary) and phosphate ions Question: The critical pH in the oral cavity that results in demineralization of tooth enamel and release of calcium phosphate is 1. pH 5.5 2. pH 6.3 3. pH 7.2 4. pH 9.2 Acidogenic Theory of Caries: Diet Diet selects for the growth of certain microbial species ◆ Availability of fermentable sugars drives the ecological shift from neutral to “cariogenic plaque”. ** Especially high sucrose diet Acidogenic Theory of Caries: Bacterial classes Definitions: Acidogenic– produce (net) acidic waste, e.g. All oral Streptococci during fermentation of available carbohydrates (i.e., anaerobic metabolism) ◆ Host diet dependent: No food = no new acid production Bacterial species in dental plaque that are especially associated with dental caries are highly acidogenic and are usually also either aciduric and/or acidophilic Acidogenic Theory of Caries: Bacterial classes Definitions: Aciduric (acid resistant) – can easily survive in acid environment, pH