10. etiology bacteria and calculus - 2023.pdf

10/2/23 1 § Periodontal infection: initiated by specific invasive oral pathogens that colonize dental plaque biofilms on the tooth root surface § This chronic challenge of virulent microorganisms leads to destruction of tooth-supporting soft and hard tissues of the periodontium § alveolar bone...

10/2/23 1 § Periodontal infection: initiated by specific invasive oral pathogens that colonize dental plaque biofilms on the tooth root surface § This chronic challenge of virulent microorganisms leads to destruction of tooth-supporting soft and hard tissues of the periodontium § alveolar bone § tooth root cementum § periodontal ligament 2 1 10/2/23 § Starts close to the time of birth (Human fetus inside the uterus is sterile) § Within hours after birth, the sterile oral cavity is colonized by low numbers of mainly facultative and aerobic bacteria 3 § The oral microbiota of newborns closely resembles the mother's vaginal microbiota or, for newborns delivered by cesarean section, the mother's skin microbiota 4 2 10/2/23 § Beginning the second day, anaerobic bacteria can be detected in the infant's edentulous mouth § Within 2 weeks, a nearly mature microbiota is established in the gut of the newborn § After weaning (>2 years), the entire human microbial flora is formed by a complex collection of approximately 1014 microorganisms consisting of more than 400 different types of bacteria 5 §From this moment on, our body contains 1.3 to 10 times more bacteria than human cells! 6 3 10/2/23 It has been estimated that, for a normal, healthy human being, the bacterial population comprises 2 kg of the total body weight. 7 § Streptococcus salivarius and Streptococcus mitis have been identified as the first and most dominant oral microbes to colonize the oral cavity of newborn infants § Veillonella , Neisseria, Actinomyces and Staphylococcus spp. are also among the first colonizers of the oral cavity § After tooth eruption, a more complex oral microbiota is established 8 4 10/2/23 Oral Dis 5:278, 1999; and Kononen E: Development of oral bacterial flora in young children. Ann Med 32:107, 2000. 9 § In general, this microbiota lives in harmony with the host, but under special conditions disease may occur § Increased mass or pathogenicity § Reduced response host 10 5 10/2/23 § All bacteria maintain themselves within their host by adhering to a surface § The ability of a bacterium to adhere to its host is crucial for the induction of infectious diseases, such as gingivitis or periodontitis Newman and Carranza's Clinical Periodontology Scanning electron micrograph of epithelial intercellular spaces that contain bacterial plaque (B) enmeshed in a fibrin-like material. C, Epithelial cells; E, erythrocyte. 11 Studies have shown high numbers of bacteria attached to pocket epithelial cells in vivo. 12 6 10/2/23 § Areas of gingival inflammation are characterized by an increased number of adhering bacteria which can also infiltrate the pocket wall in relatively large numbers and reach the underlying stroma § A positive correlation exists between the adhesion rate of pathogenic bacteria to different epithelia and the susceptibility of the affected patient to certain infections. From Nissengard RJ, Newman MG: Oral microbiology and immunology, ed 2, Philadelphia, 1994, Saunders 13 § Defined clinically as a structured, resilient, yellow-grayish substance that adheres tenaciously to the intraoral hard surfaces, including removable and fixed restorations 14 7 10/2/23 15 § Sessile microbial populations are considered to be sufficiently different from free-living microorganisms to merit their own name § Biofilms are composed of Vertical section through a 4-day human plaque sample J Dent Res 79:21, 2000 microbial cells encased within a matrix of extracellular polymeric substances, such as polysaccharides, proteins, and nucleic acids. 16 8 10/2/23 Scanning electron photomicrograph of a cross-section of cementum AP attached plaque C cementum Scanning electron micrograph of cocci and filaments associated with the surface of pocket epithelium in a case of marginal gingivitis. ×3000. 17 Predominantly grampositive attached zone. Tooth surface Sulcular epithelium Predominantly gramnegative unattached zone Courtesy Dr. J. Sottosanti, La Jolla, Calif. 18 9 10/2/23 Transport to the Surface Strong Attachment Colonization and Plaque Maturation Initial Adhesion 19 20 10 10/2/23 21 Primitive circulatory system that removes waste products and brings fresh nutrients to the deeper layers of the film 22 11 10/2/23 23 § Biofilm bacteria are often up to 1000 times more resistant to antimicrobial agents than their planktonic counterparts 24 12 10/2/23 § The intercellular matrix consists of organic and inorganic materials derived from saliva, gingival crevicular fluid, and bacterial products § Organic constituents: § § § § Polysaccharides Proteins and glycoproteins Lipid material DNA. They play a major role in maintaining the integrity of the biofilm § Inorganic components: predominantly calcium and phosphorus, with trace amounts of other minerals such as sodium, potassium, and fluoride. Source of inorganic constituents is primarily saliva. As the mineral content increases, the plaque mass becomes calcified to form calculus 25 Development of the polymicrobial biofilm The picture can't be displayed. 26 13 10/2/23 One-day-old plaque Gram-positive cocci and short rods predominate at the tooth surface Developed supragingival plaque Gram-negative rods, filaments, and spirochetes predominate in the outer surface of the mature plaque mass. § Typically demonstrates the stratified organization of a multilayered accumulation of bacterial morphotypes Courtesy Dr. Max Listgarten, Philadelphia, Pa. 27 § The microbiota differs in composition from the supragingival plaque, primarily because of the local availability of blood products and a low reduction–oxidation (redox) potential, which characterizes the anaerobic environment. § Many periodontopathogens are fastidious strict anaerobes and they find their preferred habitat in deep periodontal pockets. 28 14 10/2/23 Aggregobacter actinomycetemcomitans Porphyromonas gingivalis Prevotella intermedia Bacteroides forsythus Campylobacter rectus Fusobacterium nucleatum Spirochetes 29 Bacteriae contained in the yellow, green, and purple complexes appear to colonize the subgingival sulcus first and predominate in gingival health In contrast, orange complex bacteria are associated with gingivitis and gingival bleeding Red complex microorganisms including P. gingivalis, T. forsythensis, and T. denticola, organisms found in greater numbers in diseased sites and in more advanced periodontal disease 30 15 10/2/23 § Initial colonization appears to involve members of the yellow, green, and purple complexes along with Actinomyces species. § Members of the orange and then red complexes become more dominant. § Presence of increased levels of orange and red complexes is hypothesized to lead to a change in the habitat, manifested clinically as gingivitis. § The gingivitis in turn favors further proliferation by members of not only the orange and red complexes, but probably members of the early colonizing species as well. 31 32 16 10/2/23 33 § Aggressive pathogen periodontal § Has the capacity to invade soft tissues 34 17 10/2/23 § Lipopolysaccharide (endotoxin) § Leukotoxin (which forms pores in POSSESSES A NUMBER OF VIRULENCE FACTORS, INCLUDING: neutrophil granulocytes, monocytes, and some lymphocytes, which consequently die because of osmotic pressure) § Collagenase (destruction of connective tissue) § Protease (ability to cleave IgG) § Ability to adhere to hard intraoral surfaces and/or to the oral mucosae 35 § Aggressive pathogen periodontal § Its fimbriae mediate adhesion, and its capsule defends against phagocytosis 36 18 10/2/23 Newman and Carranza's Porphyromonas gingivalis adhesion capacity differences. § Microscopic confirmation of significant differences in the adhesion capacity of P. gingivalis (small green dots) to epithelial cells from (A) a resistant patient as compared with (B) a patient with severe periodontitis 37 § Produces a series of virulence factors, including many proteases, a hemolysin and a collagenase P. GINGIVALIS § Can inhibit migration of PMNs across an epithelial barrier and affects production or degradation of cytokines by mammalian cells § Has the capacity to invade soft tissues. 38 19 10/2/23 Tannerella forsythensis § Nonmotile, spindle-shaped, highly pleomorphic rod and a gram-negative obligate anaerobe § Produces several proteolytic enzymes that are able to destroy immuno-globulins and factors of the complement system § Also induces apoptotic cell death 39 § Short, round-ended, nonmotile, gram-negative rods § Less virulent and less proteolytic than P. gingivalis 40 20 10/2/23 § Gram-negative, cigar-shaped bacillus with pointed ends § Can induce apoptotic cell death in mononuclear and polymorphonuclear cells § Can trigger the release of cytokines, elastases and oxygen radicals from leukocytes 41 § Because fusobacteria coaggregate with most oral micro-organisms, they are believed to be important bridging organisms between the primary (early) and secondary (late) colonizers during colonization 42 21 10/2/23 § Ability to travel trough viscous environments § Migrate within the gingival crevicular fluid and penetrate both the epithelium and the connective tissue 43 § Some have the capacity to degrade collagen and even dentin SPIROCHETES § T. denticola produces proteolytic enzymes that can destroy immunoglobulins (IgA, IgM, IgG) or complement factors 44 22 10/2/23 § Comparing the microbiota in health, gingivitis, and periodontitis, the following microbial shifts can be identified: MICROBIAL SHIFT DURING DISEASE § From gram positive to gram negative § From cocci to rods (and at a later stage to spirochetes) § From nonmotile to motile organisms § From facultative anaerobes to obligate anaerobes § From fermenting to proteolytic species. 45 46 23 10/2/23 47 § Theory dating to the mid-1900s postulating that periodontal disease resulted from “the elaboration of noxious products by the entire plaque flora.” § Periodontal diseases were thought to result from an accumulation of plaque over time, eventually in conjunction with a diminished host response and increased host susceptibility with age. § When only small amounts of plaque exist, the noxious products are neutralized by the host; large amounts of plaque produce large amounts of noxious products, overwhelming the host’s defenses. 48 24 10/2/23 Some individuals with considerable amounts of plaque and calculus, as well as gingivitis, never developed destructive periodontitis FACT CHECK: THIS THEORY DOES NOT MAKE SENSE Individuals who did present with periodontitis demonstrated considerable site specificity with regard to the pattern of disease Some individuals with very little plaque had considerable periodontitis 49 § Although KEY FACT the nonspecific plaque hypothesis has been discarded in favor of other etiologic hypotheses, most of the therapeutic interventions are still based on the principles of the nonspecific plaque hypothesis 50 25 10/2/23 § Only certain plaque is pathogenic, the qualitative composition of the resident microbiota is important § Pathogenicity depends on the presence or increase in specific microorganisms, not the quantity of plaque § Acceptance of the specific plaque hypothesis was spurred by the recognition of A. actinomycetemcomitans as a pathogen in localized aggressive periodontitis 51 § The accumulation of plaque causes the inflammation of adjacent tissues (gingivitis) and other environmental changes that favor the growth of gram-negative anaerobes and proteolytic species, including periodontopathogens. 52 26 10/2/23 § Changes in the host status, such as inflammation, tissue degradation, and/or high gingival crevicular fluid flow, may lead to a shift in the microbial population in plaque. § This gradual shift in the entire microbial community, known as dysbiosis , may result in a chronic disease state such as periodontitis. 53 §Multiple etiologies are involved in development of periodontitis 54 27 10/2/23 § The bacterial biomass of human periodontitis-associated biofilms increases with increasing periodontal inflammation. § The selective outgrowth of these inflammatory pathobionts can perpetuate periodontal inflammation resulting in a vicious cycle for disease progression, where the dysbiosis and inflammation reinforce each other. Loos BG, Van Dyke TE. The role of inflammation and genetics in periodontal disease. Periodontol 2000. 2020;83:26–39 55 56 28 10/2/23 Conditions leading to periodontal tissue destruction (Cumulative Effect) Presence of Pathogenic Bacteria Bacterial Virulence Presence of Risk Factors Immune System Failure 57 PRIMARY ETIOLOGIC FACTORS Inflammatory reaction Proteolitic enzymes et collagenases Bacteria Neutrophils MMP Cytokines Fibroblastes, monocytes and epithelial cells Il 1β and Il 6 PGE2 58 29 10/2/23 Inflammatory reaction Proteolytic enzymes and collagenases MMP Cytokines Il 1β and Il 6 Loss of clinical attachment PGE2 59 60 30 10/2/23 If initial infection of plaque bacteria is not contained and progresses to periodontitis, macrophages and neutrophils play an important role in the progression of the disease 61 Poor Oral Hygiene Normal Flora Exogenous Infection LPS Pocketing & Bone Loss Antibody Response Pathogenic Flora AND Inflammation & Tissue Destruction Neutrophil Clearance YES Gingivitis & Limited Disease NO Cytokines & Inflammatory Mediators Initial periodontitis Macrophage/ Lymphocyte population Bacterial Penetration Systemic Exposure 62 31 10/2/23 Poor Oral Hygiene Normal Flora Antibody Response Pathogenic Flora Pocketing & Bone Loss Inflammation & Tissue Destruction Exogenous Infection AND + Risk Factors Genetic Traits Diabetes Smoking - Neutrophil Clearance YE S Gingivitis & Limited Disease NO Cytokines & Inflammatory Mediators + Monocyte Lymphocyte Axis Bacterial Penetration Systemic Exposure 63 64 32 10/2/23 Bacteriae Proteolitic Enzymes Collagen Breakdown Neutrophils MMP Macrophages Fibroblasts Pocket Formation PGE2 Epithelial Cells Osteoclasts Cytokines Il-1α, Il-6 Bone Resorption •Mobility •Recession •Loss of tooth Periodontitis: Cascade of Events 65 66 33 10/2/23 § Calculus consists of mineralized bacterial plaque that forms on the surfaces of natural teeth and dental prostheses 67 § Located coronal to the gingival margin § Visible in the oral cavity § White or whitish yellow in color, § Hard with claylike consistency § Easily detached from the tooth surface § Derived from salivary secretion 68 34 10/2/23 In extreme cases, calculus may form a bridge-like structure over the interdental papilla of adjacent teeth or cover the occlusal surface of teeth that are lacking functional antagonists. 69 70 35 10/2/23 71 § May rapidly recur after removal (lingual area of the mandibular incisors) § It may localize on a single tooth or group of teeth, or it may be generalized throughout the mouth 72 36 10/2/23 § Color is influenced by contact with tobacco and food pigments 73 § Located below the crest of the marginal gingiva § Not visible on routine clinical examination § The location and extent of subgingival calculus may be evaluated by careful tactile perception with a delicate dental instrument such as an explorer 74 37 10/2/23 § Typically hard and dense § Frequently appears dark brown or greenish § Firmly attached to the tooth surface Deposits of subgingival calculus usually extend nearly to the base of periodontal pockets in chronic periodontitis but do not reach the junctional epithelium. Derived from gingival exudate (seruminal calculus) § § 75 Both supragingival calculus and subgingival calculus may be seen on radiographs However, the sensitivity level of detecting calculus by radiographs is inconsistent 76 38 10/2/23 Dental calculus is primarily composed of inorganic components (70% to 90%) and the organic components constitute the rest COMPOSITION The major inorganic proportions of calculus are approximately: 76% calcium phosphate (Ca 3 [PO 4 ] 3% calcium carbonate (CaCO 3 ) 4% magnesium phosphate (Mg 3 [PO 4 ] 2% carbon dioxide, and traces of other elements such as sodium, zinc, strontium, bromine, copper, manganese, tungsten, gold, aluminum, silicon, iron, and fluorine. 77 Journal of Health Sciences & Research, July-December 2016;7(2):42-50 78 39 10/2/23 Calculus is mineralized dental plaque. FORMATION The soft plaque is hardened by the precipitation of mineral salts, which usually starts between the 1st and 14th days of plaque formation. Calcification has been reported to occur within as little as 4 to 8 hours. Calcifying plaques may become 50% mineralized in 2 days and 60% to 90% mineralized in 12 days. 79 Saliva is the primary source of mineralization for supragingival calculus SOURCE OF MINERALIZATION The serum transudate called gingival crevicular fluid furnishes the minerals for subgingival calculus 80 40 10/2/23 The calcium concentration or content in plaque is 2 to 20 times higher than in saliva. Early plaque of heavy calculus formers contains more calcium, three times more phosphorus, and less potassium than that of noncalculus formers, suggesting that phosphorus may be more critical than calcium for plaque mineralization. Calcification entails the binding of calcium ions to the carbohydrate–protein complexes of the organic matrix and the precipitation of crystalline calcium phosphate salts. CALCIFICATION Crystals form initially in the intercellular matrix and on the bacterial surfaces and finally within the bacteria. 81 Differences in the manner in which calculus is attached to the tooth surface affect the relative ease or difficulty encountered in its removal FOUR MODES OF ATTACHMENT: 1. 2. 3. 4. Attachment on organic pellicle on enamel Mechanical locking into surface irregularities, such as cemental resorption lacunae Close adaptation of calculus undersurface depressions to the gently sloping mounds of the unaltered cementum surface Penetration of calculus bacteria into cementum 82 41 10/2/23 Calculus (CA) attached to enamel (E) surface just coronal to CEJ 83 Calculus (CA) attached to to pellicle on enamel surface and cementum. 84 42 10/2/23 Calculus (CA) attached in a cemental resorption area (CR) with cementum (C) adjacent to dentin (D). 85 Undersurface of subgingival calculus (C) previously attached to the cementum surface (S). Note impression of cementum mounds in calculus (arrows). (Courtesy Dr. John Sottosanti, La Jolla, Calif.) 86 43 10/2/23 Subgingival calculus (C) embedded beneath the cementum surface (arrows) and penetrating to the dentin (D), making removal difficult. (Courtesy Dr. John Sottosanti, La Jolla, Calif.) 87 § Distinguishing between the effects of calculus and plaque on the gingiva is difficult because calculus is always covered with a nonmineralized layer of plaque Plaque Calcified Deposits 88 44 10/2/23 § Attributing to the porosity of calculus and its ability to retain bacterial antigens makes it an important contributing factor in initiating and accentuating periodontal disease progression 89 ETIOLOGIC SIGNIFICANCE The rough calculus surface may not, in itself, induce inflammation in the adjacent periodontal tissues, instead it serves as an ideal substrate for subgingival microbial colonization and also § acts as a niche which harbors bacterial plaque § acts as an irritant to the periodontal tissues § distends the periodontal pocket wall § inhibits the ingress of polymorphonuclear leukocytes. 90 45 10/2/23 POSITIVE CORRELATION TO PERIODONTAL DISEASE § A positive correlation between the presence of calculus and the prevalence of gingivitis exists but this correlation is not as great as that between plaque and gingivitis § Calculus plays a key role in maintaining and accentuating periodontal disease by withholding the plaque in close contact with the tooth surface and gingival tissue, leading to various pathological changes thereby creating areas where plaque removal is impossible. 91 § Calculus plays an important role in maintaining and accentuating periodontal disease by providing a fixed nidus for the continued accumulation of plaque and retaining it close to the gingival tissues and creating areas where plaque removal is impossible 92 46 10/2/23 In young persons, periodontal conditions are more closely related to plaque accumulation than to calculus, but the situation is reversed with age The incidence of calculus, gingivitis, and periodontal disease increases with age 93 Contaminated Root Surface 94 47 10/2/23 Although the bacterial plaque is the main etiologic factor in the development of periodontal disease, the removal of subgingival plaque AND calculus constitutes the cornerstone of periodontal therapy 95 48