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Controversies in periodontics / /certified fixed orthodontic courses by Indian dental academy


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Controversies in periodontics / /certified fixed orthodontic courses by Indian dental academy

  2. 2. CONTENTS: Introduction. Classifying periodontal diseases – a long-standing dilemma. Noninflammatory destructive periodontal disease (NDPD). Beneficial bacteria of the periodontium Periodontitis–systemic disease associations in the presence of smoking – causal or coincidental? In or out: the invasiveness of oral bacteria. Periodontal epithelium: a newly recognized role in health and disease. The role of stress in inflammatory disease, including periodontal disease. Finding genetic risk factors for periodontal diseases. The periodontal–endodontic controversy.
  3. 3. Introduction: When a thing ceases to be a matter of controversy, it ceases to be a matter of interest, William Hazlitt (1778–1830). Discussion of contending hypotheses on the nature and treatment of diseases that adversely affect the periodontium are no exception.Controversies in three general areas are: Classification of periodontal diseases and some aspects of microbial colonization. Inflammation and systemic factors, upon which recent classifications have been based. The second considers controversies in periodontal pathogenesis, including the role of bacterial invasion, periodontal epithelium, genetic factors, and stress. The third group includes clinical controversies.
  4. 4.  Grouping periodontal diseases into a widely accepted classification system has been difficult, based primarily on disputes about the etiology and pathogenesis of a clinically disparate disease process. More recent classifications have been based on relationships between an infecting pathogenic microbiota, resulting inflammation, and a susceptible host. The author notes that one of the constant historical features about classification systems is the acrimony that accompanies their modification and concludes that classification systems should be viewed as dynamic works-in-progress that need to be periodically modified.
  5. 5. Classification of periodontal diseases can be placed into three dominant paradigms: Primarily based on the clinical features of the diseases (1870– 1920). The concepts of classical pathology (1920–1970). The infectious etiology of the diseases (1970–present).
  6. 6.  Classification systems in the modern era represent a blend of all three paradigms since there is a certain amount of validity to some of the earliest thoughts about the nature of periodontal diseases. As classification systems have evolved, newer thoughts about periodontal diseases have been superimposed on a matrix of older ideas that are still considered to be valid. Only those ideas that are believed to be clearly outmoded or incorrect have been discarded. In a sense, the newest or dominant paradigm rests on a foundation of the still valid components of the older or previous paradigms.
  7. 7.  One of the interesting historical features of classification systems is the often intense resistance to their modification. Many people appear to believe that classification systems are rigid and fixed entities that should not be changed. In fact, classification systems should be viewed as dynamic works-in–progress that needs to be periodically modified based on current thinking and new knowledge.
  8. 8. CLASSICAL PATHOLOGY PARADIGM (1920–1970) As the field of periodontology began to mature scientifically in the first half of the 20th century, many clinical scholars in both Europe and North America began to develop, and argue about, nomenclature and classification systems for periodontal diseases. What emerged from this debate was the concept that there were at least two forms of destructive periodontal disease inflammatory and noninflammatory (‘degenerative’ or ‘dystrophic’).
  9. 9.  Gottlieb, in particular, had a significant influence on the field when he postulated that certain forms of destructive periodontal disease were due to degenerative changes in the periodontium. He believed that he had discovered histological evidence of impairment in the continuous deposition of cementum (i.e. ‘cementopathia’).
  10. 10. • Although most classification systems published from approximately 1920 to 1970 included a degenerative disease category at the 1966WorldWorkshop in Periodontics. Serious questions were raised about the existence of ‘periodontosis’ as a distinct disease entity.• Many recommended that the term be discarded. It was not until 1977, that meeting supported the conclusion that ‘periodontosis’ was actually an infection and ‘juvenile periodontitis’ should become the preferred term for this group of diseases.
  11. 11. • The next major discovery in periodontal microbiology was the preliminary demonstration in 1976–1977 of microbial specificity at sites with periodontosis.• This finding, coupled with the demonstration in 1977– 1979 that neutrophils from patients with juvenile periodontitis (periodontosis) had defective chemotactic and phagocytic activities, marked the beginning of the dominance of the Infection/Host Response paradigm.
  12. 12. • The next major landmark in the classification of periodontal diseases emerged from the 1989 World Workshop in Clinical Periodontics where a new classification of periodontitis based on the Infection/ Host Response paradigm was suggested by AAP.• The classification was a refinement of one that had been proposed by Page & Schroeder in 1982 and a similar one that had been adopted by the AAP in 1986.
  13. 13. Five types of destructive periodontal disease were listed:• I Adult Periodontitis.• II Early Onset Periodontitis.• III Periodontitis Associated with Systemic Disease.• IV Necrotizing Ulcerative Periodontitis.• V Refractory Periodontitis.
  14. 14. Drawbacks:• Depended heavily on the age of the affected patients.• Rates of progression.Other important features:• Periodontitis Associated with Systemic Disease.• Refractory Periodontitis category.
  15. 15. • Overlap exists among categories and cases exist that do not clearly fit into any single category.• In addition, it was acknowledged that considerable ‘heterogeneity’ existed within the Refractory Periodontitis category since, it includes patients who are unresponsive to any treatment provided whatever the thoroughness or frequency as well as patients with recurrent disease at few or many sites.• Finally, different forms of periodontitis proposed in the classification shared many microbiologic and host response features, which suggested extensive overlap and heterogeneity among the categories.
  16. 16. • As a consequence of these problems, the 1989 classification was criticized shortly after it was published and a different system was proposed by Ranney(1993). • Adult Periodontitis. • Early Onset Periodontitis • Necrotizing Ulcerative Periodontitis.• He suggested elimination of the ‘Refractory Periodontitis’ category since it was a heterogeneous group and it was impossible to standardize the treatment that necessarily would have to be given prior to making the diagnosis.• In addition, he recommended elimination of the ‘Periodontitis Associated with Systemic Disease’ category.• Since the, expression of all forms of periodontitis can be modified by some systemic diseases or abnormalities, it is probably better to consider them in that specific context, rather than treating them as a unique category.• Nevertheless, despite its problems, the classification was adopted by the world community as reflected by its widespread use in the periodontal literature.
  17. 17. • Its acceptance was facilitated by the ease with which patients could be placed into age-based categories (i.e. adult vs. early onset disease).Drawbacks:• The disease category of ‘Prepubertal Periodontitis’ was the first to be seriously questioned.• The uncertainty about the proposal that ‘Rapidly Progressive Periodontitis’ was a single entity, and secondly, the questionable criteria used to determine its presence.• Distinguish between ‘Generalized Juvenile Periodontitis’ and ‘Rapidly Progressive Periodontitis’? Since there are no definitive answers to these, and other similar questions, the classification lost some of its clinical utility.
  18. 18. 1999 CLASSIFICATION OF PERIODONTAL DISEASES AND CONDITIONS• Problems, inconsistencies, and deficiencies associated with the 1989 classification led many clinicians and investigators to call for a revision of the currently used system.• This resulted in a 1999 international workshop on the classification of periodontal diseases.• One of the goals of this workshop was to correct the problems associated with the 1989 system.
  19. 19. There were six major problems with the 1989 classification that needed to be addressed:1) It did not include a gingivitis or gingival disease category.2) The periodontitis categories had non validated age dependent criteria.3) There was extensive crossover in rates of progression of the different categories of periodontitis. Rapidly Progressive Periodontitis was a heterogeneous category.4) There was extensive overlap in the clinical characteristics of the different categories of periodontitis.5) Refractory Periodontitis was a heterogeneous category.6) Prepubertal Periodontitis was a heterogeneous category.
  20. 20. • What emerged was a classification that was even more firmly based on the Infection/Host Response paradigm, but without some of the inherent problems of the 1989 classification.• In reality, the changes could be characterized as a ‘course correction’ or ‘fine-tuning’ of the 1989 classification since no massive alterations were made.• A badly needed gingivitis or gingival disease category was added.• In addition, the heterogeneous disease categories of prepubertal, refractory and rapidly progressive periodontitis were eliminated as distinct or stand- alone entities.
  21. 21. • The ‘refractory’ designation remains in the new classification, but not as a single entity.• Changing the names of ‘Adult Periodontitis’ to ‘Chronic Periodontitis’ and ‘Juvenile Periodontitis’ to ‘Aggressive Periodontitis’ was made.• These changes were specifically made to eliminate the non validated age-dependent designations.
  22. 22. PERIODONTAL- ENDODONTIC CONTROVERSY: Over the past century the dental literature has consistently reflected a controversy related to the effect of periodontal disease on the dental pulp and more recently the effect of pulpal necrosis on the initiation and progression of marginal bone loss is dealt. Two basic questions have been raised and continue to be matters of dispute. Is periodontal disease a cause of pulp necrosis? Can a pulpless tooth be the cause of periodontal disease? The answers to these basic questions are of utmost clinical importance.
  23. 23. • Most histological interpretations of the past decades have suggested that the dental pulp resides in a rather precarious environment.• Even some current texts list a litany of ills which may befall a pulp from exposure to periodontal disease and subsequent periodontal treatment.• Such projections, however, fail to recognize more recent physiological data which demonstrate that the pulp has a quite sophisticated vasculature for such a relatively primitive tissue.
  24. 24. • Vast networks of capillary beds have been demonstrated as well as sophisticated control systems including precapillary sphincters and arteriovenous shunts have been noticed.• An active lymphatic system has also been demonstrated.• As the effectiveness of a tissue’s vasculature is key to its adequate function, such physiological observations suggest that the dental pulp has mechanisms which provide a significant capacity for survival.
  25. 25. The Effects of Periodontal Disease and Procedures on the Dental Pulp:• Over the years there has been a consistent stream of speculation as to the effect of periodontal disease on the dental pulp.• Recent publications have suggested that ‘periodontal disease’ is a ‘direct cause of pulpal atrophy and necrosis’ (Petka K 2001), ‘periodontal disease’ is ‘more deleterious to the pulp than both caries and restorations combined’ (Petka K 2001), and ‘periodontal disease and periodontal treatments should be regarded as potential causes of pulpitis and pulpal necrosis’ (Wang et al 2002).• Such interpretations have little basis in current scientific fact, but do demonstrate the persistence of an often repeated point of view in literature.• A review of recent studies related to the ‘periodontal– endodontic’ controversy therefore seems in order.
  26. 26. The pathways for communication and extension of disease from a periodontal pocket to the pulp are:• Through patent dentinal tubules.• Lateral canals.• Apical foramen or foramina. Demonstration of the presence of such pathways is commonly identified as evidence that specific periodontal disease must have some effect on the health of the dental pulp.
  27. 27. • The following histological and clinical studies suggest, however, that such relationships rarely, if ever, result in pulp necrosis.• Kirkham BD (1975) examined 100 periodontally involved teeth and found that only 2% had lateral canals located in a periodontal pocket.• Tagger M & Smukler H (1977) removed roots from molar teeth so extensively involved with periodontal disease that root amputation was required, and found that none of the pulps of the resected roots showed inflammatory changes.• Haskell et al (1980) also removed roots from maxillary molars with total or nearly total periodontal involvement and found no inflammatory cells or very few inflammatory cells present in the pulps of the periodontally involved resected roots.
  28. 28. • Czarnecki & Schilder (1979) performed a histological study of intact, caries-free teeth and compared the pulps of teeth which were periodontally within normal limits with teeth which had periodontal disease.• The pulps in the intact, caries-free, periodontitis group were all histologically within normal limits regardless of the severity of the periodontal disease.• In the same study they found that only teeth with extensive decay or extensive restorations showed evidence of pulp pathosis.• Jaoui et al (1995) studied patients with advanced periodontal disease for 5–14years after completion of active periodontal treatment.• Of the 571 teeth that did not have root canal treatment at the time of completion of periodontal treatment, only one tooth (0.175%) required root canal treatment over the 5- to 14-year recall period.
  29. 29. • The cause of pulp necrosis could be identified by the clinicians in most cases. Recurrent decay resulting in pulp exposure was the primary cause.• Extension of periodontal disease to involve the root apices is also cited as a reason for root canal treatment, but it is not known if the pulps of these teeth were in fact necrotic or whether root canal treatment was accomplished to facilitate additional periodontal treatment.• But few of the teeth requiring root canal treatment were listed as having unknown cause.
  30. 30.  In summary, unless periodontal disease extends all the way to the tooth apex, the weight of evidence in the literature suggests that the dental pulp is capable of surviving significant insults and that the effect of periodontal disease as well as periodontal treatment on the dental pulp is negligible. It also appears that the clinical significance of the relationship between periodontal disease and the dental pulp has been greatly exaggerated in historical and much of the current periodontal–endodontic literature.
  31. 31. The Effects of Endodontically Involved Teeth on Periodontal Health and Healing:• Historically the effect of periodontal disease on the dental pulp has been a source of discussion for the better part of the past century.• Only in recent years has the reverse been discussed.• The potential effect that a tooth with a necrotic pulp or a tooth that has had root canal treatment may pose as a risk factor:• In the initiation and progression of periodontal disease.• Resolution of periodontal pockets.
  32. 32. • The projected negative effects of pulpless teeth appear to be based on studies related to the similarity of the microbial flora in root canals and deep periodontal pockets, negative effects on periodontal healing in replantation studies, and a series of retrospective statistical studies by Jansson, Ehnevid, Lindskog and Blömlof (1993).• The presumed pathway is primarily through patent dentinal tubules.• The clinical consequences suggested by series of studies are significantly deeper probing depths, more bone loss, impaired periodontal healing following nonsurgical periodontal treatment, and enhanced progression of periodontal disease.
  33. 33. • Jansson et al (1993) conducted a study in a smaller group to evaluate intraindividual comparisons and reports a mean pocket depth difference of 0.27mm to 0.66mm in five tooth groups and 0.98mm in a sixth group with or with out pulpal involvement.• In a second paper Jansson et al (1993) state, ‘Mean probing depths for each tooth were approximately 0.2mm deeper in teeth with the same degree of radiographic attachment in the presence of angular destructions when periapical pathology was present compared to teeth without periapical pathology’.
  34. 34. • Study, Jansson & Ehnevid (1998) evaluated the periodontal status of mandibular molars.• They reported that the mean periodontal probing depth of a nonroot-filled molar with a periapical lesion was 0.7mm deeper than corresponding teeth with no periapical lesions, and that the mean probing depth difference at proximal sites was 0.2mm.• It is quite curious to note that they found that molars with root canal fillings, but no evidence of periapical pathosis, were not significantly correlated to periodontal probing depth or to degree of furcation involvement.• In summary, while it has been suggested that a pulpless tooth may represent an etiological risk factor related to periodontal disease, the comparative risk must be considered negligible based on clinical outcomes.
  35. 35. NONINFLAMMATORY DESTRUCTIVE PERIODONTAL DISEASE:• Prior to the 1970s, the causes and pathobiology of periodontitis in humans were not understood, and no widely accepted system of nomenclature and classification of periodontal diseases existed.• The large number of suspected causes included local irritation from calculus, rough or overhanging restoration margins, or ill-fitting oral appliances, systemic diseases and conditions, diet and nutrition, abnormal occlusal forces, were considered.• By the 1970s, the central role of bacteria in causing periodontitis had been documented, and concepts about the nature of periodontal disease had begun to shift from those of classical pathology to the infectious/host defense paradigm.
  36. 36. • Destructive periodontal disease is infectious, and they are all characterized by chronic inflammation, pocket formation and progressive deepening, and loss of attachment and alveolar bone.• Author suggest the existence of at least one form of severe destructive periodontal disease that is not recognized in the recent classifications.• In this form of periodontal disease, loss of attachment, resorption of alveolar bone and tooth loss occur, but gingival inflammation and pocket formation and deepening are not prominent features.• Antimicrobial therapy is not effective in arresting or slowing the progress of the disease and bacteria may not be the primary cause.
  37. 37. • A noninflammatory form of destructive periodontal disease was first described by Hunter in 1771 and subsequently confirmed by Fox (1832), Gottlieb (1932) and Orban (1942).• A category of noninflammatory destructive periodontitis was included in the first AAP classification of periodontal diseases in 1942, and was an integral part of virtually all subsequent classifications published up to about 1970.
  38. 38. • The disappearance of NDPD from the literature occurred concurrently with increasing documentation of the important role of bacteria in the etiology of periodontitis and the shift in concepts about periodontal diseases from the Classic Pathology paradigm to the Infection/Host Defense paradigm as described by Armitage (2002).• Under the latter paradigm, all forms of destructive periodontal disease were considered to be infectious and to be characterized by inflammation, pocket formation and loss of periodontal attachment and alveolar bone.
  39. 39. NDPD has several distinct diagnostic characteristics:• Generalized loss of attachment.• Resorption of alveolar bone.• Extensive gingival recession, affecting many teeth, without formation of deep periodontal pockets or significant clinical manifestations or history of gingival inflammation,• Occurring in individuals with excellent daily oral hygiene.• The disease is recognized most frequently in individuals in their 30s or 40s, although it may begin in patients in their 20s.• It may affect all of the teeth or it may be more severe around the posterior or the anterior teeth.
  40. 40. • NDPD may be a noninfectious form of periodontal destruction.• Analysis of the plaque flora fails to reveal the presence of expected putative periodontal pathogens such as P. gingivalis, B. forsythus, A. actinomycetemcomitans, and T. denticola or enteric bacterial species.• Furthermore, serum antibody analyses generally fail to reveal evidence for prior periodontal infection.
  41. 41. • There is abundant evidence that periodontitis, as the disease is traditionally defined, is caused by specific bacteria that extend apically between the gingiva and tooth surface to cause inflammation, formation of periodontal pockets with a pocket epithelium and destruction of the periodontal ligament, the gingival connective tissue and the alveolar bone.• Inflammatory macrophages and granulocytes which become activated to produce large quantities of cytokines, especially interleukin-l (IL-1), tumor necrosis factor-a (TNF-a) and prostaglandins, and members of a large family of enzymes known as the matrix metalloproteinases (MMP).
  42. 42. • Although the mechanisms underlying NDPD have not been directly investigated, author suggest that they may be the same as for periodontitis except that the production of prostaglandins and MMP, as described above, may be initiated and perpetuated by factors other than bacterial infection.• The mediators may be produced by cells that are normally resident in the periodontal tissues rather than infiltrating inflammatory cells.• Fibroblasts plus a few macrophages (histiocytes) comprise the predominant cell population present in noninflamed gingiva (Schroeder HE 1973).
  43. 43. • These cells could become activated to produce, cytokines, prostaglandins and MMP by application of abnormal forces as well as by binding of IL-l, TNF-α, or bacterial substances.• Such forces could originate from enduring, frequently applied aggressive oral hygiene.• The resident fibroblasts could therefore serve as a source of molecules that mediate resorption of the alveolar bone and destruction of gingival and periodontal ligament connective tissues.• Based on the above hypothesis, author have focused on the idea that soft tissue trauma resulting from aggressive daily oral hygiene combined with a possible genetically determined enhanced susceptibility could account for the pathobiology of NDPD.
  44. 44. • In summary, over a period of more than 30years of practice, author have encountered a large number of cases of destructive periodontal disease that do not fit the diagnostic criteria of any form of periodontal disease described in the classifications published since the 1970s.• The primary diagnostic features of the disease include progressive gingival recession and loss of periodontal attachment and alveolar bone, the absence of gingival inflammation and microbial deposits and periodontal pocket formation, and failure of the disease to respond to traditional antimicrobial periodontal treatments.• In addition, the disease appears to be noninfectious.• To distinguish the disease from various forms of periodontitis, author suggests the name Non- inflammatory Destructive Periodontal Disease.
  45. 45. BENEFICIAL BACTERIA OF THE PERIODONTIUM:• Author proposes that bacteria and their products are a necessary and beneficial component of a healthy periodontium.• The primary evidence for their hypothesis is that clinically healthy periodontal tissue contains a highly orchestrated gradient of selected inflammatory mediators that plays a key role in the defense of this tissue and the overall health of the individual.
  46. 46.
  47. 47. • Extensive culture studies by Moore et al found certain species, including Actinomyces, Streptococcus, and Veillonella to be associated with health while more gram-negative species, Treponemes, and higher numbers of Fusobacterium nucleatum were associated with disease.• Socransky et al found that many of the bacterial taxa appeared to cluster together including those associated with gingival health.• His green cluster included Capnocytophaga species, Campylobacter concisus, Eubacteria nodatum and Streptococcus constellatus.
  48. 48. • The yellow cluster was formed by a group of streptococci, and the purple cluster included Actinomyces odontolyticus and Veillonella parvula.• These species tended to occur together in the periodontal crevice and did not associate with increasing pocket depth or gingival bleeding.• Interestingly, in other studies the species from those clusters associated with periodontal health were found to be unaffected or even increased following scaling and root planing and periodontal maintenance procedures.
  49. 49. • Recently, Ximenez-Fyvie et al (2000) examined supra and subgingival plaque in clinically healthy subjects and in periodontitis patients for the same 40 bacterial taxa in a DNA checkerboard analysis and found similar species in both supra and subgingival plaque samples from healthy and diseased sites.• However, they observed a higher mean prevalence of the Actinomyces species in health, with the diseased (deeper) sites tending to have higher counts of bacteria overall as well as greater proportions of the more pathogenic ‘orange’ and ‘red’ complexes of bacteria including Bacteroides forsythus, Porphyromonas gingivalis, Treponema denticola, and Prevotella intermedia.
  50. 50.
  51. 51. • Certain periodontal pathogens, such as P. gingivalis, are adapted to survival in the pocket.• Their outer membrane lipopolysaccharide is capable of downregulating E-selectin and interleukin-8.• Thus potentially interrupting the local inflammatory response.• This helps the bacteria to avoid elimination while maintaining deeper inflammation that provides the organism with needed nutrients in the form of increased crevicular fluid flow and blood products from the ulcerated pocket epithelium.
  52. 52. • In summary human beings generally do well with regards to their periodontal status because we have co-evolved with the commensal bacteria that serve to protect us through promotion of a beneficial host response.• However, this host-bacterial balance is dependent on the specific genetic markers of each individual (major histocompatibility complex type, gene polymorphisms, etc.), environmental factors (smoking, stress, etc.), and the continually evolving microbial community.• A more thorough understanding of these factors should lead to improved periodontal health in the twenty-first century.
  53. 53. PERIODONTITIS–SYSTEMIC DISEASE ASSOCIATIONS IN THE PRESENCE OF SMOKING – CAUSAL OR COINCIDENTAL?• Individuals with periodontitis are more likely to be current or past cigarette smokers than individuals without periodontitis (Hujole PP et al 2002).• Therefore, when individuals with and without periodontitis are compared it is to be expected that individuals with periodontitis will have more smoking-related diseases, such as coronary heart disease, lung cancer, low-birth weight babies etc., than individuals without periodontitis.• The comparison between individuals with and without periodontitis with respect to the occurrence of systemic diseases is said to be biased because of the unequal distribution of smoking in the two groups.
  54. 54. • In epidemiological terminology, smoking is referred to as a confounder factor.• Statistical adjustment or control for confounding is possible using different statistical methods such as stratification or covariance adjustment in statistical models.• Such statistical adjustment can be used to eliminate some but not all of the bias caused by the higher prevalence of smokers among individuals with periodontitis.• The goal of statistical adjustment is to make the two compared groups (individuals with and without periodontitis) similar with respect to the true lifelong exposure to any form of tobacco smoking.
  55. 55. Periodontitis and smoking are associated with similar health risks:• Smoking is most strongly associated with lung cancer, followed by COPD, CHD and stroke. Smoking is associated with a decreased risk for Parkinson’s disease.• Periodontitis mimics this pattern step by step: periodontitis is most strongly associated with lung cancer, followed by COPD, CHD and stroke.• If periodontitis–systemic disease associations are a result of incomplete adjustment for smoking, other periodontitis–systemic disease associations should become predictable. Because smoking is negatively associated with Parkinson’s disease, periodontitis should be also.
  56. 56. • There have been a total of nine cohort studies published on the periodontitis–CHD associations.• Four of the nine studies had poor smoking adjustment, while five had good smoking adjustment.• Periodontitis was not significantly associated with CHD (HR 1.05; 95% confidence interval 0.96–1.15) among those studies that provided a good adjustment for smoking dose.• In contrast, periodontitis was significantly associated with CHD in the four studies that either did not adjust for smoking or adjusted crudely (HR 1.25; 95% confidence interval 1.15–1.37).
  57. 57. • Lack of control for smoking dose provides a plausible explanation for why small, but statistically significant, periodontitis– CHD associations are only present for studies that poorly adjust for smoking.• In summary the possibility of smoking– periodontitis interactions cannot be excluded.• Periodontitis may cause systemic diseases only in the presence of smoking; or, periodontitis may worsen the ill effects of smoking on systemic health.
  58. 58. IN OR OUT: THE INVASIVENESS OF ORAL BACTERIAINVASION OBSERVED IN VIVO:The concept that oral bacteria can penetrate the gingiva extendsback to at least the beginning of the twentieth century whenGoadby (1907) proposed that bacteria can invade oral tissues.Later cultural and histological studies provided experimentalsupport; however, being sustained only by sporadic reports in theliterature.In 1965 Listgarten used electron microscopy to observe gingivaltissue from cases of acute necrotizing ulcerative gingivitis, thereby beginning a new era of research into tissue invasion.Listgarten reported the presence of spirochetes and fusiforms inthe necrotic zone overlying ulcerated lesions and also observed adeeper zone beneath the surface of the ulcerated region thatcontained only spirochetes.
  59. 59. • The application of immunofluorescence and immunohistochemical staining provided a means to identify the invading bacteria. P.g, P.intermedia, A.a and A. naeslundii were all recorded within gingival tissues, with their presence being a characteristic of diseased sites.• Up to this juncture the term ‘invasion’ was taken to mean intercellular penetration, i.e. bacteria locating between the host cells.• Although as early as 1974 Takarada et al noted that invasion ‘into the superficial epithelial cells was occasionally encountered’, it was not until intracellular invasion (i.e. bacteria locating within epithelial cells) became established as an important property of enteropathogens, that researchers seriously considered this possibility for oral pathogens.• Rudney et al. (2001) employed fluorescent in situ hybridization (FISH) in combination with CSLM to examine buccal epithelial cells. Both A.a and P.g, along with other unidentified species, were found in high numbers within these cells taken from 23 of 24 healthy subjects.
  60. 60. Porphyromonas gingivalis:• Is a gram-negative anaerobe.• Strongly associated with severe manifestations of periodontal disease and possesses a vast array of virulence factors.• In terms of invasion of epithelial cells, two invitro models have been used extensively, namely primary cultures of gingival epithelial cells (GEC) and transformed oral epithelial cells such as the KB cell.• Invasion of GEC by P. gingivalis is swift and profuse. Within 15min of exposure, high numbers of P. gingivalis cells are located intracellularly, predominantly in the perinuclear area.
  61. 61. • The bacteria are not constrained by membranous vacuoles and can remain viable for extended periods.• The invasive process, represented schematically, begins with the proximal association between P. gingivalis cells and GEC.• Under these conditions P. gingivalis is induced to secrete a novel set of extracellular proteins, including homologs of a phosphoserine phosphatase and a polysaccharide biosynthesis enzyme.
  62. 62.
  63. 63. Actinobacillus actinomycetemcomitans: Predominant pathogen in localized juvenile periodontitis, the invasive properties of the gram negative capnophile A.a are under active investigation. Bacterially driven internalization within KB cells was first reported by Taylor’s group in 1991 and uptake is now understood to be a dynamic multistep process, as schematically represented. Initial adhesion to the epithelial cell transferrin receptor appears to be the primary stimulus for invasion, although binding to integrins may constitute a secondary entry pathway. Attachment induces effacement of the microvilli and the bacteria enter through ruffled apertures in the cell membrane.
  64. 64.
  65. 65. PERIODONTAL EPITHELIUM: A NEWLY RECOGNIZED ROLE IN HEALTH AND DISEASE:• The epithelium has an active role in keeping the periodontium healthy, as shown by its effective barrier function, its production of antimicrobial peptides, and its role in chemokine and cytokine expression in response to environmental stimuli.• In a state of health, our epithelial barriers and our innate defenses are extremely effective. When these first-line defenses are impaired, the acquired immune system serves as the back-up mode of defense.• In the past, research has focused on the destruction of connective tissue and on the acquired immune response in periodontal disease. With emerging evidence of the role of innate immunity, it is time to look at the other side of the story and to understand the periodontal epithelium and its important role in maintaining health and communicating environmental dangers before they get out of hand.
  66. 66.
  68. 68.
  69. 69. STRESS AND PERIODONTAL DISEASE:• Stress, a term continually being redefined in the scientific study of disease and illness, is nevertheless a confirmed and important factor in the etiology and maintenance of many inflammatory diseases, including periodontal disease.
  70. 70. Evidence for the role of stress in periodontal disease:• In a review of psychosocial factors in inflammatory periodontal disease reported in 1995 Monteiro da Silva et al distinguish between acute necrotizing ulcerative gingivitis and adult periodontitis, concluding that the evidence is strong for stress as a predisposing factor to acute necrotizing ulcerative gingivitis, while the evidence for psychosocial factors as etiological agents in periodontitis is not as substantive.
  71. 71. • Evidence for a relationship between psychosocial stress, coping in response to stress, and periodontal disease was also observed in a cross-sectional epidemiological study of 1426 adults, aged 25– 74years by (Genco RJ 1999).• Results indicated a significant role for financial strain in relation to greater alveolar bone and periodontal attachment loss, after adjusting not only for age and gender, but also for smoking.• Interestingly, those individuals with a problem- solving coping style for managing the stressors of daily living fared better than those who exhibited a more emotionally focused and less adequate coping response to psychosocial strain.
  72. 72. • Deinzer et al (1999) report an experiment to assess the relationship between academic stress and gingival inflammation, assessing changes in IL- 1β, a component of the immune system thought to play a role in periodontal tissue destruction.• Using a split mouth design, medical students voluntarily neglected oral hygiene of two quadrants for 21days, to induce an experimental gingivitis in those quadrants, while maintaining high levels of oral hygiene in the remaining two quadrants.• It was observed that examination students showed significantly higher levels of IL-1β at both the experimental gingivitis sites than the sites of good oral hygiene.• Indicating that stress may affect periodontal health through suppressed immune system activity, and that such a relationship would be more pronounced when oral hygiene was not maintained.
  73. 73. • Machtei et al (1992) conducted one year follow up study who demonstrated further periodontal attachment loss after 1-year.• Immune system response was examined for level of serum IgG antibody to three periodontal pathogens, Bacteroides forsythus, P. g, and A.a.• Significantly elevated odds ratios (OR) for cases was associated with IgG for Bacteroides forsythus, P. g, and A.a.
  74. 74. REFERENCE:• Periodontology 2000, Vol. 30, 2002, 7–8• Periodontology 2000, Vol. 30, 2002, 9–23• Periodontology 2000, Vol. 30, 2002, 24–39• Periodontology 2000, Vol. 30, 2002, 40–50• Periodontology 2000, Vol. 30, 2002, 51–60• Periodontology 2000, Vol. 30, 2002, 61–69• Periodontology 2000, Vol. 30, 2002, 70–78• Periodontology 2000, Vol. 30, 2002, 79–90• Periodontology 2000, Vol. 30, 2002, 91–103• Periodontology 2000, Vol. 30, 2002, 123–130