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. INTRODUCTIONWhen a thing caeses to be a matter of controversy, it caeses to be a matterof interest.In reviewing past and present concepts and treatment modalities that areavailable, it becomes evident that there are no completely acceptedprinciples and techniques.On this note, I would like to present my topic for seminar:CONTROVERSIES IN PERIODONTICS.
  3. 3. VIRAL— BACTERIAL INTERACTIONS IN PERIODONTITIS Recent studies have demonstrated various human viruses, especially cytomegalo. viruses and Epstein Barr Viruses type 1, seem to play a part in pathogenesis of human periodontitis. Parra and Slotes reported that HCMV was present in 60 % of patients and EBV- IN 30%. Slots examined frequency of HCMV, EBV-2 and herpes simplex Viruses in subgingival samples. They reported 89% of samples yielded atleast one of three test viruses from deep periodontal pockets and 56% yielded from shallow periodontal pockets
  4. 4. Dual virus infection seems to be particularly pathogenic and they may accentuate bacterial virulence factor.HCMV resides in monocytes, macrophages, and T cells and EBV in B cells, which has the potential to impair major defense mechanism of the periodontium.Tiny et al. reported that high rate of active HCMV infection in early localized aggressive periodontitis.They suggested that puberty is an important for HCMV and EBV primary infection or reinfection.Puberty related perturbation of immune system
  5. 5. CMV has been shown to lead decreased Polymorphonuclear Leukocytechemotaxis, phagocytosis, oxidative burst and intracellular killing capacity and itmay increase the human susceptibility to bacterial infection. HCMV infection of monocytes macrophage can induce prostaglandin E2 production that may result in increased bone resorption and suppressed Tlymphocyte function.Mac Donald et al. emphasize the possible detrimental role of HCMV and EBV-1 inperiodontal repair.   Bacterial infection and other condition that promote diapedesis ofinflammatory cells in a tissue would increase possibility of initiating an HMCVinfection of the tissue.
  6. 6. Contreras et al. in 1999 conducted a study to examine relation ship between subgingival herpes virus and periodontal disease and periodontopathogenic bacteriaThe study confirmed positive relationship between subgingival EBV-1, HCMV and mixed herpes viral infections and clinical severity of periodontitis.Viral infection promote subgingival pathogenic bacterial infection than vice versa. Neutrophil dysfunction may serve to potentiate over growth and virulence of P gingivalis and other microbes.
  7. 7. WIDTH OF THE KERATINIZED GINGIVA Attached gingiva is firm, resilient and tightly bound to underlyingperiosteum of alveolar bone. Distance between mucogingival junction and projection on external surfaceof the bottom of the gingival sulcus   Keratinized gingiva includes marginal gingiva also.   No standard width of keratinized gingiva has been established.   It may be necessary to increase zone of healthy tissue if it is subjected totrauma of the prosthetic treatment.
  8. 8. For many years the presence of adequate zone of gingiva was considered critical for maintenance of marginal tissue health and for prevention of continues loss of connective tissue attachment.Narrow zone of gingiva --1) was in sufficient to protect periodontium from injury caused by frictional forces encountered during mastication and to dissipate the pull on the gingival margin created by muscles of adjacent alveolar mucosa.2) it will favor sub gingival plaque formation3) it will also favor attachment loss and soft tissue recession
  9. 9. Goldman and Cohen outlined a tissue barrier concept Dense collagenous band of connective tissue retards or obstructs the spread of . inflammation better than does the loose fiber arrangement of the alveolar mucosa. Limits recession as result of inflammation This view is indirectly supported by findings of Kennedy et al.after recall evaluations of u patients from their 6 years longitudinal study of free autogenous gingival grafts ADEQUATE WIDTH OF GINGIVA Some authors suggested that less than 1 mm. Apicocoronal height ought to exceed 3 mm Third category of authors stated that adequate zone of gingiva is any dimension of gingiva which --- 1) is compatible with gingival health or 2) prevents retraction of gingivalmargin during movements of the alveolar mucosa.
  10. 10. Lang and Loe conducted a study to evaluate the significance of the gingival zone. The results showed that despite of the fact that tooth surfaces were free from plaque, all sites with less than 2 mm exhibited persisting clinical signs of inflammation.. In contrast teeth possessing least attached tissue s (cuspid and bicuspids) are least involved periodontally as compared to molars. Incidence of disease is greater on palatal and lingual surfaces of molars where amount of keratinized tissue is greatest Wenstrom and Lindhe have shown that a free gingival unit supported by a looselyattached alveolar mucosa is not more susceptible to inflammation than a free gingivalunit that is supported by a wide zone of attached gingiva..
  11. 11. • Miyasato et al. (1997) ceased oral hygiene for a period of 25 days and found no difference in development of clinical signs of gingival inflammation between areas with minimal and those with appreciable width of gingiva.• Dorfman et al. examined 96 patients with bilateral side facial tooth surfaces exhibiting minimal keratinzed tissues, which has been treated with free gingival graft on one side and un treated control on other side.• Width of keratinized gingiva on grafted site was increased to 4mm following the treatment.• The attachment level at grafted sites and control remained unchanged through out the years.• Thus narrow zone of gingiva has the same resistance to continues attachment loss as wider zone of gingiva.
  12. 12. TRAUMA FROM OCCLUSION. What is occlusal trauma? The international workshop for classification of periodontal disease and conditions in 1999. Occlusal Trauma - It is injury resulting in tissue changes within attachmentapparatus as a result of occlusal forces. Primary Occlusal Trauma – Injury resulting in tissue changes from excessive occlusal forces applied to a tooth or teeth with normal support. Secondary trauma from occlusion – Injury resulting in tissue changes from normal or excessive occlusal forces applied to a tooth or teeth with reduced support.
  13. 13. Role of occlusion in pathogenesis of periodontal disease Occlusal trauma is associated with periodontal disease over 100 years. In 1901 Karolyi ,in 1917 and 1926 Stillman indicated that excessive occlusalforce was the primary cause of periodontal disease.These early reports created a background for controversy that continues to this day. Is there association between excessive occlusal forces and progression ofperiodontal disease? At what point does an occlusal force become excessive.When should treatment initiated and how should this treatment initiated and how should this treatment accomplished?
  14. 14. Several early authors felt that occlusal forces were the initiating factor in periodontal disease and led to ongoing progression of periodontal lesion. In an attempt to demonstrate this relationship several animal studies on sheep and monkeys were conducted   Later some investigators state that traumatic occlusion causes changes in attachment apparatus without involving gingival unit.They postulated that change in attachment apparatus is mainly due to reducedblood supply to periodontal ligament
  15. 15. Orban and Weinmann in 1933 using human autopsy material evaluated .They concluded that there was no relation ship between excessive occlusal force and periodontal destruction.Instead they suggested that gingival inflammation extending in to supporting bone was the cause of periodontal destruction During the same time Glickman and co workers published studies.These studies demonstrated a phenomenon described as an altered pathway of destruction when an excessive occlusal force was present.Change in orientation of gingival and periodontal fibersCo destruction.Vertical osseous defectsBased on this observation, use of occlusal adjustment was advocated as part of the treatment of existing periodontal disease, Occlusal adjustment to prevent periodontitis was not advocated
  16. 16. Waertaug evaluated large number of human autopsy specimens to determine relationship of morphology of osseous defect and excessive occlusal forces. No relation between excessive occlusal force and vertical bone loss. Polson and Lindhe conducted studies to evaluate effect of plaque and excessive occlusal forces in animal models. These studies agreed removal of plaque and control of inflammation would stop. progression of periodontal disease whether or not excessive occlusal forces are present. Meitner reported when squirrel monkeys was subjected to repeated mechanical injury in combination with marginal periodontitis, the connective tissue loss was not greater than that of specimen in which periodontitis alone was induced. Thus these appeared to be no co destructive effect on connective tissue attachment.
  17. 17. PROBLEM IN RELATING FINDING FROM ANIMAL RESEARCH TO THE HUMAN DENTITIONAn ideal model on which to study occlusion is not yet to be found.If a high crown on tooth of a dog or monkey, the tooth will intrude and recognize a new position while human tooth gets progressively mobile. Parafunctional habit is a major factor in human occlusal trauma, monkeys and dogs not known to have such persistent habits   Periodontal disease naturally occurs in humans. In the animals models the lesion of periodontal is induced artificially. With treatment these artificially treated lesion repair more predictably than naturally occurring lesions•
  18. 18. PERIODONTAL – ENDODONTIC CONTROVERSY• Two questions have been raised and continue to be matters of dispute.• 1) Is periodontal disease a cause of pulpal necrosis?• 2) Can a pulpless tooth be cause of periodontal disease?
  19. 19.  The effect of periodontal disease and procedures on the dental pulp
  20. 20. Periodontal diseases• Recent publications have suggested that periodontal disease is a direct  cause of Pulpal atrophy and necrosis. • The  pathways  for  communication  and  therefore  for  the  extension  of  disease  from  a  periodontal  pocket  to  pulp  are  through  patent  dentinal  tubules, lateral canals, and apical foramina. • Many  histological  and  clinical  studies  suggest,  however,  that  such  relationships rarely, if ever, result in pulp necrosis.
  21. 21. • Kirkham examined 100 periodontally involved teeth and found only 2% had  lateral canals located in a periodontal pocket. • Tagger & Smukler removed roots from molar teeth so extensively involved  with periodontal disease that root amputation was required, and found that  none of the resected roots showed inflammatory changes. • Haskell  et  al  also  removed  roots  from  maxillary  molars  with  periodontal  involvement and found no inflammatory cells or very few inflammatory cells  present in the pulps of the periodontally involved resected roots.
  22. 22. •   Czarnecki    &  Schilder  performed  a  histological  study  of  intact,  caries  free  teeth and compared the pulp of teeth, which had periodontal disease.  The  pulp    of  the  periodontally  involved  teeth  were  all  histologically  similar  to  caries free teeth .  Teeth  with  extensive  decay  or  extensive  restortations  showed  evidence  of  pulpal pathosis. • Ross & Thompson evaluated the progress of 100 patients with maxillary molar  furcation involvement over a period of 5—24 years.   Of  the  387  maxillary  molars,  79%  had  at  least  50%  or  less  bone  support  around one root prior to periodontal treatment. Only  4%  required  root  canal  treatment  subsequent  to  periodontal  therapy.  None  were ascribed to the effects of advanced periodontal disease in pulp.
  23. 23.   Jaoui  et  al.  studied  patients  with  advanced  periodontal  disease  for  5—14  years after completion of active periodontal treatment . Of the 571 teeth that did not have root canal treatment at time of completion  of periodontal treatment, only one tooth required root canal treatment over  the 5 to 14 year recall period.  Pulpal insult through patent dentinal tubules or the occasional exposed lateral  canal  have  relatively  insignificant  effect  on  the  ability  of  the  dental  pulp  tissue to survive.
  24. 24. Periodontal procedures• The clinical research studies by Ross Thompson, Bergenholtz , Nyman  and  Jaoui  et  al  evaluated  patients  who  presented  with  advanced  periodontal disease, received periodontal treatment. • They  received follow up maintenance for periods ranging from 4 to 24  years. There were 1,623 teeth in the combined studies • Four  percent  required  root  canal  treatment  subsequent  to  periodontal  treatment, and follow up periodontal care. • Cause of pulp necrosis was mainly due to pulpal exposure. • Extension of periodontal disease to involve the root apices is also cited  as a reason for root canal treatment
  25. 25. • In summary dental pulp is capable of surviving significant insults and  that the effect of periodontal disease as well as periodontal treatment is  on the dental pulp is negligible.  • The weight of evidence in literature shows that clinical significance of  the relationship between periodontal disease and dental pulp has been  exaggerated in historical and much of the current periodontal – endodontic literature
  26. 26. Effect of endodontically involved teeth on periodontal health and healing. Only in recent years the potential effect of a tooth with a necrotic pulp or  a tooth that had root canal treatment was considered as a risk factor in  the initiation of periodontal disease. • Pulpless  tooth  with  a  periapical  lesion  promotes  the  initiation  of  periodontal  pocket  formation  and  interfere  with  healing  of  periodontal  lesion after periodontal treatment.  Jansson et al. state that teeth teeth with periapical lesion had lost more  proximal bone . 0.19  mm  year  vs  0.06mm  year  for  teeth  with  no  periapical  lesion  or  where there is evidence of reduction in lesion size.
  27. 27. • Sanders et el. reported in 1983 that after the use of freeze – dried bone  allografts  65%  of  teeth  that  did  not  have  root  canal  treatment  showed  complete or greater than 50% bone fill in periodontal osseous defects. • While  only  33%  of  teeth  which  had  root  canal  treatment  prior  to  periodontal surgical procedure had complete or greater 50% bone fill.
  28. 28. ROLE OF LYMPHOCYTES IN PERIODONTITIS•   Inflammatory  cells,  predominantly  lymphoid  cells  and  macrophages  thought to be engaged in controlling bacterial challenge. • Participation  of  these  cells  in  a  major  way  in  process  of  tissue  destruction had not yet been conceived.• In  1970  antibodies  to  cell  surface  markers  became  available  which  allowed sub categorization of T lymphocytes in to two major subsetsCD4  and CD8.• CD4 molecules serves as a co receptor for major histocompatibility class  .  two molecules on antigen presenting cells.  • CD8 molecule is a co receptor for MHC class one molecules of the target  cells.
  29. 29. Phenotypic Analysis• Phenotypic analysis shows that there are no numerical abnormalities of  T helper cells or major cells. • There  may  be  altered  ratios  of  CD4  to  CD8  in  periodontal  lesions  of  aggressive periodontitis patients
  30. 30. Functional studies• T and B-lymphocytes are present in lesions of early onset periodontitis  patients. • Two accepted activities of the lymphocytes are. 1) They may provide protection against host from infectious agents.2) they contribute to host tissue damage.  B cells and their linear descendents secrete immunoglobulins (IgG) that  may  inactivate  bacterial  toxins,  prevent  bacterial  adherence  and  promote bacterial phagocytosis by polymorphonuclear leukocytes.
  31. 31.    Juvenile periodontitis patients frequently have elevated levels of serum  IgG antibodies against AA antigens. • But still there has been controversy that whether these antibodies were  protective or not.• IgG2 antibodies are the predominant sub class presented. • IgG2 antibodies are not been thought to be effective direct opsonins, or  activators of direct classical pathway. • IgG2 antibodies can kill AA only when neutrophil has the proper allotypic  form of fc receptor.  • Abnormal lymphocyte function in early onset periodontitis as manifested  by lower than normal levels of non stimulated DNA synthesis in cultured  peripheral blood mononuclear cells. • This reaction has been called autologous mixed lymphocyte function  (AMLR )
  32. 32. • In some of the studies of periodontal disease patient AMLR returned to  normal after periodontal treatment. • It  is  not  known  how  diminished  AMLR  relates  to  early  onset  periodontitis.It  has  been  suggested  that  reduced  AMLR  relate  to  improper regulation of B cell responses. • In  1974  Langer  et  al.  reported  that  peripheral  blood  lymphocyte  from  juvenile  periodontitis  patients  exhibited  reduced  blastogenic  response  to dental plaque and gram –ve bacteria. • Several other studies following this early reports found that lymphocytes  from  periodontitis  patients  exhibited  more  exacerbated  than  normal  blastogenic response to mitogens and bacterial antigens. • This phenomenon remains with no strong scientific evidence although it  may  be  related  to  reduce  AMLR  via  reduced  population  of suppressor  inducer T cells.
  33. 33. ROOT - CONDITIONING•   Exposed  root  surface  as  result  of  periodontitis  has  undergone  substantial  alteration  and  may  no  longer  serve  as  an  appropriate  substrate for cell attachment. • Loss  of  collagen  fiber  insertion,  contamination  of  root  surface  by  bacteria and alteration in mineral density. • Root surface also lack chemotactic stimuli for migration of cell capable  of producing periodontal regeneration. • Apical  migration  of  junctional  epithelium  along  root  surface  over  connective  tissue  following  surgical  therapy  also  appear  to  inhibit  regeneration
  34. 34. • Scaling and root planning is effective in removing bacterial deposits as well  as removing endotoxins from exposed root surface. • How ever it results in formation of smear layer is thought to serve as a  physical barrier between periodontal tissues and root surface and may  inhibit formation of new connective tissue attachment to root surface.•  Root conditioning of these periodontally involved root surface will eliminate  cytotoxic materials, will dematerializes the planed root surface,will also  expose and enlarge opening of dentinal tubules and will dematerializes the  inter tubular dentin.•  Exposed collagen matrix of dentin is chemotactic for PMN, macrophage  and fibroblasts. • It can also support the attachment and migration of fibroblast. • Root surface demineralization will also enhance healing
  35. 35. HISTOLOGICAL AND CLINICAL SUTDIES• College  of  dentistry  --Columbus  asses  the  efficacy  of  root  surface  biomodification through tetracycline citric acid or EDTA in patients with  chronic periodontitis. • They included all the studies evaluating histological and clinical effects  of citric acid, tetracycline and EDTA. • They excluded studies evaluating effects of extra cellular matrix protein,  enamel matrix protein or growth factors applied to root surface.
  36. 36. Main results• Thirty-four  studies  incorporating  total  patient  population  of  575  were  analyzed, 26 for citric acid, 5 for tetracycline and 3 EDTA treatment. • Four  of  eight  human  histological  studies  represents  regeneration  with  use  of  citric  acid  and  only  1  of  18  clinical  studies  reported  attachment  gain. • Of 5 studies using tetracycline, 1 histological study and 1 clinical study  reported attachment gain. • No regeneration was reported in the 3 studies evaluating use of EDTA.
  37. 37. Reviewer’s conclusion• Evidence to data suggests that use of citric acid, tetracycline and EDTA to modify root surface provides no benefit of clinical significance to regeneration in patients with chronic periodontitis
  38. 38. Root conditioning delays wound healing?• Selvig et al. examined wound healing in experimental fenestration defects following conditioning of defects walls with either saline or citric acid.• Following elevation of mucoperiosteal flaps, fenestral defects where covered with polytetrafluroethylene membrane.• Post surgically after 14 days healing appears to be delayed in citric acid treated site as compared to the control.
  39. 39. RESTORATION OR IMPLANT PLACEMENT: A growing treatment planning quandaryRegardless of the implant system, the placement and functional success of endosseous implants is greater than 90%.Is a tooth with questionable prognosis restored or intervened with dental implant?Should a tooth with large post and core restoration and failing endodontic procedure is re treated conventionally or should it be extracted?Is it better to replace such a tooth with an implant?If the implants fail to integrate or if restoration is an esthetic failure, would it have been better to retain the tooth?Answering such questions is a challenge for clinicians. Clinical and economic factors should be considered in making such decisions.
  40. 40. Clinical factors The heavily restored tooth• These teeth may have been restored multiple times, have minimal external coronal dentin for an adequate restorative ferrule.• The post space can be so large that internal dentinal walls of the preparations are too thin.• If greater force is to be exerted on a tooth, increase in the resistance form should be made.• Crown lengthening can increase resistance but at the expense of removing bone of adjacent teeth.• Orthodontic extrusion can also be considered but extrusion adds both additional financial cost and increased time to treatment.
  41. 41. Immediate implant placement along with single stage surgical placement limits number of procedures.Before the acceptance of sinus augmentation procedures, the choice might have been to retain teeth with root resective and endodontic re treatment procedures.Previously it was thought that implants in posterior maxillae or mandible was less ideal..Decision for implant placement may change if patient is a heavy smoker or if they are an uncontrolled diabetic, factors which could compromise implants
  42. 42. The Furcation involvement• Reducing attachment levels for crown lengthening or for root resective procedures may have a negative long-term impact.• Periodontally involved molars are the most common teeth lost.• Furcation and concavities associated with them make them difficult to treat.• Resecting roots can improve debridement acess but literature differs as to success of root amputations or hemi–sections.• Reasons for failures were current decay, endodontic failure,root fractures and less commonly, recurrent periodontal dis• Resection may require osseous removal to the adjacent teeth, as crown lengthening does.• If osteoplasty ostectomy is not performed then plaque – retentive areas are created
  43. 43. Hemi–section• Hemi–section, the length of root trunk affects how much bone is removed to create positive osseous architecture.• To create a positive osseous architecture a large amount of bone must be removed on remaining root and adjacent tooth..• If the patient’s anatomy requires sinus augmentation, then clinician may reconsider treating tooth with root resection.
  44. 44. Difficult anterior esthetic cases• The use of dental implants to replace anterior teeth is one of the last areas to gain acceptance by dental profession.• The greatest benefit is avoidance of unnecessary preparations of non- restored teeth adjacent to an implant.• Professional acceptance of implants in esthetic zone has increased because they are• Better pre-surgical planning guidelines.• More option in diameter of implants fixtures.• Great variety of abutments.• Better techniques for preparing edentulous ridge.• Better prosthetic techniques to produce a high esthetic final restoration.
  45. 45. ECONOMIC FACTORS• Clinician as well as patients many times elects best economic option than best treatment option.• Some still argue that the long-term success rates of implants are not high enough and that questionable teeth should be maintained until they become hopeless.
  46. 46. Hand versus Ultrasonic Instrumentation• Partial removal of cementum became established as a therapeutic procedure over one century ago.• Mergenhen and Hampp were the first to demonstrate that plaque – related gram-negative bacteria produce the complex lipo-polysachride endotoxins described by Boe in 1941• Aleo and De Renzius scientifically proved the significance of root cementum bound endotoxin removal in periodontally diseased teeth.• In 1974 they showed that cementum of these involved teeth contains endotoxins and also found that this lipo-polysachride is toxic to cells in vitro.
  47. 47. Comparison• Many investigators have compared hand and ultrasonic instrumentation.• Nishimine and O’ Leary showed that root planning was more effective than ultra sonic scaling in removing endotoxins from periodontally involved root surfaces.• Two investigations evaluated the smoothness of root surfaces at an ulrtastructural level following hand and ultrasonic instrumentation.• One study reported a much smoother root following ultrasonic scaling. The second study reported opposite results.• Luiggi and Gian conducted a study to compare efficacy of ultrasonic and hand instrumentation.• They found no significant differences between fibroblast growth on periodontally involved root surfaces treated with hand instruments and with sonic scalers.
  48. 48. • Several studies reported on an increased efficiency of subgingival instrumentation with both sonic and ultra sonic scalers, since manual instrumentation takes longer to achieve the same clinical results (Dargoo 1992,Copulos et al. 1993).• Power driven instruments have been shown to be superior in treatment of class 2 and class 3 furcations (Leon & Vogel 1987).• Development of heat at scaler tip when water-cooling is not sufficient. This increased temperature may cause injury to pulpal and periodontal tissues.• Another draw back is formation of pathogenic bacterial aerosols and the reduced tactile sensation in comparison to hand instruments.
  50. 50. NONSURGICAL PERIODONTAL THERAPY• Conventional nonsurgical periodontal therapy consists of mechanical supra and subgingival tooth debridement• Reducing the bacterial load and altering the microbial composition towards a flora more associated with health,which in turn result in lower levels of inflammation and relative stability in periodontal attachment levels.• In the past, endotoxin or lipopolysacchairde derived from cells of gram-negative bacteria was though to be so firmly attached to the root surface.• More recent studies on extracted teeth indicate that endotoxins are superficially bound and can be removed by such means as brushing.• Thus systematic root planing to remove cementum does not seem warranted.
  51. 51. • Furcation opening is often less than 1 mm, too small to be effectively reached with relatively larger curettes.• Most of the new ultrasonic tips are approximately 0.50mm in diameter, which may favor ultrasonics as the instruments of choice for furcation sites.• One study on instrumentation of furcations with and without surgical access indicates that no major differences were observed between use of curettes or ultrasocics in the closed treatment groups and in wide furcations.
  52. 52. PERIODONTAL SURGERY• The following have been proposed as the aims of periodontal surgery:• Accessibility to previously in accessible root surfaces.• Production of healthy dento-gingival junction that would enable the patient to practice a high level of plaque removal.• Reduction of probing depths to allow - a) effectively delivered maintenance and home care and b) the monitoring and or diagnosis of recurrent inflammation and progressive periodontal disease.
  53. 53. COMPARISON OF SURGICAL AND NONSURGICAL TREATMENT MODALITIES• An early study employing a split-mouth design was that of knowles et al.. Three modalities were tested sub-gingival curettage, modified Widman flap surgery and pocket elimination surgery• After evaluation for eight years all techniques resulted in favorable changes in the means of the clinical parameters measured• The surgical techniques resulted in slightly more pocket reduction in deep pockets.• The modified Widman flap resulted in the greatest clinical attachment gain.• In studies comparing the effects of root planing and modified Widman flap surgery over 6 years of observation,.• The modified Widman flap resulted in more pocket reduction in initially deep pockets, although mean attachment levels were similar.
  54. 54. In summary, following points may be deduced from available literature.• Both non-surgical and surgical therapies have been shown to result in similar mean improvements of clinical scores.• Data for the possible adjunctive effect of surgical procedures on patients/sites unresponsive to initial therapy are scarce.• Data for the possible adjunctive effect of surgical procedures on patients believed to be at high risk to ongoing attachment loss are scarce.• Other than studies on regenerative techniques data for the comparable effects of different surgical modalities on furcation areas are also scarce.• Data for long-term outcome measures, such as tooth loss and quality of life issues, are scarce.
  56. 56. • No Current issue in periodontal research is more visible or controversial than the relationship between periodontitis and systemic diseases.• Four lines of evidence suggests that the observed periodontitis-systemic disease associations are in part a result of confounding by smoking• First, no periodontitis-systemic disease associations have been identified among neversmokers.• Second, periodontitis and smoking mimic one another with respect to the types of diseases with which they are associated (e.g. lung cancer and Parkinson’s disease).• Third, only studies with inadequate adjustment for smoking report significant periodontitis-systemic disease associations.• Lastly, elimination of dental infection, unlike smoking cessation, does not reduce coronary heart disease risk.
  57. 57. Smoking, the epidemoiologists’ perspective• Individuals with periodontitis are more likely to be current or past cigarette smokers.• When individuals with and without periodontitis are compared it is to be expected that individuals with periodonititis will have more smoking- related diseases, such as coronary heart disease, lung cancer, low-birth weight babies etc.,..• Statistical adjustment of control for confounding is possible.• Such statistical adjustment can be used to eliminate some but not all of the bias caused by the smokers.
  58. 58. • The imperfect smoking questionnaires,the inability to ask questions or otherwise obtain information on important characteristics of smoking, all make it virtually impossible to have perfect statistical adjustment for smoking.• Wherever past or current smokers are included in the analyses, biased periodontitis – systematic disease associations will be reported.• Therefore, primary analyses should be limited to healthy never-smokers both because smoking is such a strong risk factor and because the magnitude of smoking cannot be well measured.
  59. 59. Effect of smoking on Periodontitis cannot be distinguished from the effect of smoking on systemic diseases• Periodontitis-systemic disease associations have not been identified among never-smokers.• Periodontitis and smoking are associated with similar health risks.• Conflicting study results can be explained in terms of statistical adjustment for tobacco smoking.• Dental infection elimination through complete tooth removal, unlike smoking cessation, does not reduce health risks.
  60. 60. Periodontitis and chronic obstructive pulmonary disease (COPD)• Among past and current smokers, periodontitis significantly increased the risk for COPD.• When the analysis included past, current, and never smokers with adjustment for reported smoking dose and duration, the HR for COPD decreased by 7%.• Finally, when the analysis was limited to never-smokers, periodontitis was associated with a small and insignificant increased risk for COPD.
  61. 61. Periodontitis and lung cancer• Among past and current smokers, periodontitis significantly increased the risk for lung cancer• When the analysis included never, past, or current smokers, with adjustment for smoking the HR for lung cancer associated with periodontitis decreased by 49%.• When the analysis was limited to never-smokers, the opposite association was present.• Periodontitis was associated with a decreased risk for lung cancer, not an increased risk.
  62. 62. Periodontitis and stroke• Among past and current smokers, periodontitis marginally increased the risk for stroke.• When the analysis included never, past or current smokers with adjustment for smoking, the HR for stroke associated with periodontitis decreased by 8%.• Finally, when the analysis was limited to never-smokers, periodontitis increased the HR for stroke by 11%.• These findings differ from previously reported results.
  63. 63. Periodontitis and coronary heart disease (CHD)• Among past and current smokers, periodontitis significantly increased the risk for CHD by 26%.• Among past, current and never-smokers the HR for CHD associated with periodontitis was 1.13.• Finally, when the analysis was limited to never-smokers, the HR for CHD associated with periodontitis became insignificant).• Imperfect adjustment for smoking history is inducing associations between periodontitis and smoking related diseases.
  64. 64. • There is also hope that periodontal treatments can reverse an increased CHD risk..• Findings from the same cohort study indicated that complete elimination of all dental infections by extraction does not decrease CHD risk..• Then why would an incomplete, imperfect and reversible decreasing of the bacterial load by means of periodontal treatments decrease CHD risk?• Some have offered the explanation that the risk, once established, is not reversible and therefore primary periodontitis prevention trials rather than secondary prevention should be initiated.
  65. 65. Conflicting study results can be explained in terms of statistical adjustment for tobacco smoking• Study was categorized as having good adjustment for smoking when the number of cigarettes smoked per day was taken into account in the analyses.• When a study did not take into account the number of cigarettes smoked per day the study was categorized as poorly adjusted.• There have been a total of nine cohort studies published on the periodontitis-CHD associations.• Periodontitis was not significantly associated with CHD 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.
  66. 66. Dental infection elimination through complete tooth removal does not reduce health risks• There is certainly hope that secondary prevention of CHD events can occur through periodontal treatment.• Current epidemiological evidence does not support the hope that periodontitis plays a role in secondary heart disease prevention.• A cohort study in the US population suggests that periodontitis does not increase the risk for secondary heart disease events.• Individuals with periodontitis and pre-existing heart disease were found to be at the same risk for developing a secondary heart disease event as the individuals with pre-existing heart disease but without periodontitis.
  67. 67. • There is also hope that periodontal treatments can reverse an increased CHD risk..• Findings from the same cohort study indicated that a definitive, irreversible, and complete elimination of all dental infections by extraction does not decrease CHD risk.• Then how incomplete, imperfect and reversible decreasing of the bacterial load by means of periodontal treatments decrease CHD risk?• Some have offered the explanation that the risk, once established, is not reversible and therefore primary periodontitis prevention trials rather than secondary prevention should be initiated.
  68. 68.
  69. 69. THANK