Critical issues in periodontal research /certified fixed orthodontic courses by Indian dental academy


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Critical issues in periodontal research /certified fixed orthodontic courses by Indian dental academy

  1. 1. Critical Issues In PeriodontalResearch INDIAN DENTAL ACADEMY Leader in Continuing Dental Education
  2. 2. Introduction
  3. 3. Epidemiology and Prevalence : 50s and the 60s Russel’s Periodontal Index Ramfjord’ Periodontal Index Common pattern of prevalence.
  4. 4. Gingivitis Early teenage years and diminished in the late twenties/thirtiesPeriodontitis Late teenage percentage of persons involved increases rapidly ( >90% in the middle age ) Once initiated pdtitis progressed in a continuous and linear pattern till tooth loss. ( Greene, 1963 )
  5. 5.
  6. 6. 1980s.. National Survey of Americans ( 18-65 years ) 14%-16% ( 45 years or >) One or more pockets 6mm or deeper Presence of periodontitis not extensive ( Brown & Loe 1993 )
  7. 7.
  8. 8. Brown et al 1990 attachment loss of 5 mm or > --- < 1 % all sites studied. deep pockets < 1% of the sample studied
  9. 9. Less plaque & calculus – less incidence of periodontitis.Baelum 1986 -Villagers in Zanzibar & Pemba islands(Tanzania) - High levels of plaque & calculus - less than 10% with 5mm or > attachment loss - less than 10% of sample with 3mm or deeper (Reddy et al 1986 South Africa)
  10. 10. 3 issuesIs the prevalence changing? implications on dental education, practice , public health.A small percentage of the sample studied afflicted with the disease Identity & characteristics of this section 90%-5% Identification of determinants of disease resistence & susceptiblity
  11. 11. good oral hygiene = periodontal health? poor or no oral hygiene = severe periodontitis? (Brown & Reddy 1986)
  12. 12. Microbiology :1960s Forsyth Dental Center, Boston, USA (pioneer studies on periodontal microflora) Diseased site plaque : quantity of plaque higher with predominance of Gram negative anaerobic species. P. gingivalis
  13. 13. Jordan & Keyes 1964 Periodontitis : an infectious transmissible disease(rodents with a “form of disease” with alveolar bone loss) Loe & Coworkers 1965First direct evidence , human study Lindhe et al animal model, periodontitis is of bacterialorigin 1970s Consensus of bacterial infection
  14. 14. Consensus : disease of bacterial origin Microbial Plaque of Any composition (non-specific plaque hypothesis) specific plaque hypothesis (1976 Walter Loeshe)Recognition of A.actinomycetemcomitans asthe pathogen causing Aggressive Periodontitis
  15. 15. Etiologicagents Haffajee & Socransky 1994
  16. 16. Periodontitis : A sequential infection? (Williams et al 1985) Species A causes disease Mounts a host response Arrest of progressionSuppression below disease causing levels Recurrence of disease with species B Repetition of cascade Numerous antibodies to antigens
  17. 17. Periodontitis is a Gram Negative Anaerobic infection. Common factor or “shared characteristic” : Lipopolysaccharides McCoy et al 1987 LPS ;lipid A, core carbohydrate, oligosaccharide side chains. Be concerned with the LPS & details of the organism producing it may be irrelevant.
  18. 18. Periodontitis : A)consequence of overgrowth of commensals or an B)exogenous origin?A)Factors determinig the overgrowth at some sites in some indidviduals. Trasmission not an issueB) Factors bringing about transmission a)Presence of putative pdl pathogens in healthy sites Socransky et al 1991 Dahlen et al 1989 b) Aa & P gingivalis transmitted among family members
  19. 19.
  20. 20. Microbial testing Repeat Microbial
  21. 21. Viruses in Periodontal disease : Association between a bacterial infection and viral disease. Reduce PMN chemotaxis, phagocytosis,Respiratory burst. Dual infections with HCMV and EBV– increased risk of periodontal breakdown.
  22. 22. Bacterial infectionsrelease of inflammatory cells (PMNls etc) Triggering of viral infctions Viruses reside in the inflammatory cells Treat the bacterial infection Diminished viral countsReduced inflammatory cells
  23. 23. Pathogenesis : 1960s : focus on the bacterial effect on the host 1970s : focus on the host factorIvanyi and Lehner 1970 peripheral blood mononuclear cells sensitised to antigens of infecting bacteriaLavine 1976 discovery of defective neutrophils (less chemoattractant reaction)Mediators Of Inflammatory Response PGs, cytokines , chemokines (Stolman J, Maderazo 1976) MMPs (Reynolds)
  24. 24. Pathways : Normal individual Plaque accumulation Chemoattarctants like IL-8 produced (vascular inflammation) E-selectin Neutrophil binding
  25. 25. Primary host CR3 defens eSusceptible individualsmacrophages take
  26. 26. Disease Health IL-1beta, TNF-alpha, TNF-gamma,PGE2 ,MMPs high low IL-4,IL-10,TGF-beta,IL-1ra,TIMPs low high
  27. 27. Environmental and acquired risk factors Cytokns prostnoids PMns Antbdy Host Connective Clinical signsMicrobial Immuno Tissue and of diseasechallenge Inflammatory MMPs host & antigns response metabolism progression LPS Genetic risk factors KORNMAN & LOESCHE 1997
  28. 28. Page 1991,
  29. 29. Susceptibility : Genetic based and Risk basedGenetic factors :Susceptibility : variation in normal genetic sequences e.g. polymorphism in the gene encoding forIL-1alpha, beta … increased severity of the disease. EOP : possible genetic risk factor
  30. 30. Criticisms of the lack of logic in polymorphism association studies Periodontitis (Condition A) Loss of bone (abnormality B) Bone loss due to osteoclast affected by gene C Association of the gene C with a known polymorphism D Kinane & Hart 2005
  31. 31. Diagnosis : 60s & 70s : presence of pocket : tantamount to having periodontitis. disease progression : continuous & linear 80s Episodic , site specific and infrequent. Some sites – disease inactive disease active Inability to distinguish between the two entities
  32. 32. Diagnosis : Until 1980s… LJP & Chronic Marginal Periodontitis Periodontitis : homogenous disease Family of closely related diseases withdiffering natural histories, responses to therapyand prognoses. 1983 1989 1999
  33. 33. Essentialism & Nominalism : Essentialism : Definition of a disease : “ X is a…..” merely confirming the existence of X the disease. The essentialists hankering after a unified concept of diseases asa class of agents causing illness, is mistaken and misleading for severalgood reasons: many diseases remain of unknown cause; known causesare of diverse types; causation may be complex, with interplay of severalfactors, intrinsic; and, more generally, an effect – the disease – should notbe confused with its own cause’. Scadding
  34. 34. “ …The names of diseases are a convenientway of stating briefly the endpoint of a diagnosticprocess that progresses from assessment ofsymptoms and signs towards knowledge ofcausation.” Scadding Set of criteria : if fulfilled …. Come to adiagnosis.Periodontitis : more of a syndrome than adisease Complex etiology and a cluster of signs &symptoms van der Velden 2005
  35. 35. Classification of pdl disease in exhaustive and exclusive way.Based on ageBased on extent of the disease ( number of teethaffected )Based on severity ( CAL and PD)Based on clinical characteristics van der Velden 2000
  36. 36. Radiographs :Standard recommendation for initial examination of a periodontitispatient A full-mouth periodontal probing complemented by a full-mouth set of intraoral radiographs. OPG & limited number of IOPAs under-overestimate the extent of disease OPG 1% of initial vertical lesions 4% IOPAs. Best radiographic technique : minimum exposure digital Imaging : not any more superior than film basedradiographyAim : detect hard tissue changes but… using underexposed, serial radiograph with CADIA mayreveal supracrestal soft tissue changes
  37. 37. Radiographs are not included in the periodontal chart : e.g. CAL , PD , Bleeding on probing -Use the CEJ as a reference point and measure distance for the alveolar crest - combine or superimpose radiographic info and clinical probing Comprehensive periodontal chart Urs Bragger 2005
  38. 38. Normative reference value for a disease temperature > 37.7°c… feverNormal Periodontium : Strictly no pockets above 3mm arbitrary values and define periodontal pockets
  39. 39. NHANES III 28 year old : 2 pockets > 5mm –destructive PDL disease 58 year old: 5 pockets > 5mm
  40. 40. Risk based reference values Body mass index> 28 …obese FBS > 126mg/dl diagnostic of diabetes 140/90 mmHg diagnostic of cardiovascular disease.Steep increase of these “surrogate markers” is related to adverse health outcomes. Pocket Depth associated with an adverse outcome : tooth loss
  41. 41. Assessment of Risk factors in Diagnosis. 1980sWhen destruction was considered linear and continuous … The only relevant risk factors ;To be an adult and human!!Small proportion of population: severe periodontitis (15%). factors affecting this kind of susceptibility : risk factors
  42. 42. Risk Factors :
  43. 43. multiple risk factors ; Beck et al 1990 persons using tobacco (risk factor 1) had higher P gingivalis counts 2% more(risk factor 2) not been to the dentist in 3 or more (RF 3) 500 times more susceptible to severe periodontal destruction
  44. 44. Systemic diseases predisposed forperiodontal disease : Vice versa : Pdl disease predisposing tosystemic diseases. DeStefano et al 1993 9760 subjects 14 years 25 % increased risk for developingCHD
  45. 45. Issues in therapy 1960sSurgical therapy : elimination of pockets and restoration of normal physiological contour 70s Techniques were honed to perfection late 70s Is Surgery inevitable…? ) Knowles et al 1979 early 80s SRP was shown to be effective in arresting the progress of the disease (Pihlstrom 1983, Baderstein et al 1984) Lindhe et al Thoroughness of debridement was more important than the treatment modality used to achieve worldwide boom in nonsurgical therapy
  46. 46. 1980sGuided Tissue Regeneration (Gottlow et al)Bone grafts Page 1993 (questions of predictability) These modalities usually fail where there is no alternate therapy available which would succeed and usually succeed where another modality would have succeeded anyway Growth factors
  47. 47. Issue of non-responding patients and periodontal vaccines : Caton 1989 (AAP) Periodontitis : infectious disease host mounts an immune response and arrest & clearing of the infection. a) are antibodies produced to infecting antigen ? b) are they protective ? SRP results in bacteremia A form of vaccination against initiation & progression of the disease?Immune response in a treated patient better than the one produced during spontaneous infection
  48. 48. non-responding patients : unable mount an immune response. Perrson et al 1994macaca fascicularis injected with a dead bacterial strain Cessation of alveolar bone lossPharmacotherapy in periodonticsLDD : delivery of the drug at high concentration for longer periods directly to the pocketsAntibiotics as adjuncts to mechanical therapy (empirical)
  49. 49. Others :Biphosphonates (inhibition of osteoclast function)NSAIDS (Inhibition of arachidonic acid pathway) Drugs of tetracycline class CMTs (MMPs) SDD (subantimicrobial dose doxycycline ) Periostat 20 mg of Doxycycline Drugs enhancing the antiinflammatory cytokines and lipoxins are also underway
  50. 50. Conclusion :As the quest to better understand periodontal disease intesifies … There are more questions than that can be answered effectively. Resolution of a few issues …. Emergence of bigger and more challenging questions.