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Critical Issues In Periodontal
Research




     INDIAN DENTAL ACADEMY
      Leader in Continuing Dental Education

     www.indiandentalacademy.com
Introduction




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Epidemiology and Prevalence :

    50s and the 60s
    Russel’s Periodontal Index
    Ramfjord’ Periodontal Index
    Common pattern of prevalence.




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Gingivitis
   Early teenage years and diminished in the late
 twenties/thirties
Periodontitis
    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 )


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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 )




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Brown et al 1990
   attachment loss of 5 mm or > --- < 1 % all sites
 studied.
    deep pockets < 1% of the sample studied




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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)




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3 issues

Is 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


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good oral hygiene = periodontal health?
 poor or no oral hygiene = severe
 periodontitis?
                  (Brown & Reddy 1986)




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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



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Jordan & Keyes 1964
 Periodontitis : an infectious transmissible disease
(rodents with a “form of disease” with alveolar bone loss)
   Loe & Coworkers 1965
First direct evidence , human study
   Lindhe et al animal model, periodontitis is of bacterial
origin

  1970s Consensus of bacterial infection




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Consensus : disease of bacterial origin

   Microbial Plaque of Any composition
    (non-specific plaque hypothesis)



                                    specific plaque hypothesis
                                       (1976 Walter Loeshe)


Recognition of A.actinomycetemcomitans as
the pathogen causing Aggressive Periodontitis




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Etiologic
agents




                               Haffajee & Socransky 1994

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Periodontitis : A sequential infection?
                            (Williams et al 1985)
      Species A causes disease

                                       Mounts a host response


        Arrest of progression
Suppression below disease causing levels

                                   Recurrence of disease with species B


        Repetition of cascade

                                   Numerous antibodies to antigens


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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.
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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 issue
B) 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


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Microbial
                               testing




                                Repeat
                               Microbial
                                testing



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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.




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Bacterial infections

release of inflammatory cells (PMNls etc)


        Triggering of viral infctions



                                  Viruses reside in the inflammatory cells


                           Treat the bacterial infection

                                              Diminished viral counts
Reduced inflammatory cells

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Pathogenesis :
  1960s : focus on the bacterial effect on the host
 1970s : focus on the host factor
Ivanyi and Lehner 1970 peripheral blood mononuclear
 cells sensitised to antigens of infecting bacteria
Lavine 1976 discovery of defective neutrophils (less
 chemoattractant reaction)
Mediators Of Inflammatory Response
  PGs, cytokines , chemokines (Stolman J, Maderazo
 1976)
   MMPs (Reynolds)
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Pathways :
 Normal individual

                                     Plaque accumulation


      Chemoattarctants like IL-8 produced
         (vascular inflammation)

                                            E-selectin



   Neutrophil binding




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Primary
                               host
                     CR3
                              defens
                                 e




Susceptible individuals
macrophages take over
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Disease                                                Health
                 IL-1beta, TNF-alpha,
               TNF-gamma,PGE2 ,MMPs
      high                                      low




             IL-4,IL-10,TGF-beta,IL-1ra,TIMPs
      low                                       high




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Environmental and acquired risk factors


                                   Cytokns
                                   prostnoids
            PMns
            Antbdy       Host                   Connective   Clinical signs
Microbial              Immuno                   Tissue and    of disease
challenge           Inflammatory    MMPs           host             &
            antigns
                      response                  metabolism   progression

            LPS




                            Genetic risk factors

                                             KORNMAN & LOESCHE 1997
                     www.indiandentalacademy.com
Page 1991, Birkadel-Hansen1993

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Susceptibility :
    Genetic based and Risk based

Genetic factors :
Susceptibility : variation in normal genetic sequences
 e.g. polymorphism in the gene encoding for
IL-1alpha, beta … increased severity of the disease.
   EOP :
     possible genetic risk factor




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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

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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

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Diagnosis :
  Until 1980s…
       LJP & Chronic Marginal Periodontitis
   Periodontitis : homogenous disease
        Family of closely related diseases with
differing natural histories, responses to therapy
and prognoses.
  1983
  1989
  1999



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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 as
a class of agents causing illness, is mistaken and misleading for several
good reasons: many diseases remain of unknown cause; known causes
are of diverse types; causation may be complex, with interplay of several
factors, intrinsic; and, more generally, an effect – the disease – should not
be confused with its own cause’.

                                                 Scadding


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“ …The names of diseases are a convenient
way of stating briefly the endpoint of a diagnostic
process that progresses from assessment of
symptoms and signs towards knowledge of
causation.”
                                Scadding
  Set of criteria : if fulfilled …. Come to a
diagnosis.
Periodontitis : more of a syndrome than a
disease
   Complex etiology and a cluster of signs &
symptoms
                               van der Velden 2005

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Classification of pdl disease in exhaustive

           and exclusive way.
Based on age
Based on extent of the disease ( number of teeth
affected )
Based on severity ( CAL and PD)
Based on clinical characteristics
                      van der Velden 2000



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Radiographs :
Standard recommendation for initial examination of a periodontitis
patient
          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 based
radiography


Aim : detect hard tissue changes
      but… using underexposed, serial radiograph with CADIA may
reveal supracrestal soft tissue changes


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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

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Normative reference value for a disease
         temperature > 37.7°c… fever


Normal Periodontium : Strictly no pockets above
 3mm
  arbitrary values and define periodontal pockets




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NHANES III
 28 year old : 2 pockets > 5mm –destructive PDL disease
  58 year old: 5 pockets > 5mm




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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



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Assessment of Risk factors in Diagnosis.
   1980s
When 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


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Risk Factors :




            www.indiandentalacademy.com
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




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Systemic diseases predisposed for
periodontal disease :
   Vice versa : Pdl disease predisposing to
systemic diseases.
  DeStefano et al 1993
      9760 subjects
      14 years
      25 % increased risk for developing
CHD




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Issues in therapy
   1960s
Surgical 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

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1980s
Guided 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


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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



                 www.indiandentalacademy.com
non-responding patients : unable mount an immune
 response.
   Perrson et al 1994
macaca fascicularis injected with a dead bacterial
 strain                   Cessation of alveolar bone loss
Pharmacotherapy in periodontics
LDD : delivery of the drug at high concentration for
 longer periods directly to the pockets
Antibiotics as adjuncts to mechanical therapy
 (empirical)


               www.indiandentalacademy.com
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



               www.indiandentalacademy.com
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.




             www.indiandentalacademy.com

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

  • 1. Critical Issues In Periodontal Research INDIAN DENTAL ACADEMY Leader in Continuing Dental Education www.indiandentalacademy.com
  • 2. Introduction www.indiandentalacademy.com
  • 3. Epidemiology and Prevalence : 50s and the 60s Russel’s Periodontal Index Ramfjord’ Periodontal Index Common pattern of prevalence. www.indiandentalacademy.com
  • 4. Gingivitis Early teenage years and diminished in the late twenties/thirties Periodontitis 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 ) www.indiandentalacademy.com
  • 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 ) www.indiandentalacademy.com
  • 8. Brown et al 1990 attachment loss of 5 mm or > --- < 1 % all sites studied. deep pockets < 1% of the sample studied www.indiandentalacademy.com
  • 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) www.indiandentalacademy.com
  • 10. 3 issues Is 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 www.indiandentalacademy.com
  • 11. good oral hygiene = periodontal health? poor or no oral hygiene = severe periodontitis? (Brown & Reddy 1986) www.indiandentalacademy.com
  • 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 www.indiandentalacademy.com
  • 13. Jordan & Keyes 1964 Periodontitis : an infectious transmissible disease (rodents with a “form of disease” with alveolar bone loss) Loe & Coworkers 1965 First direct evidence , human study Lindhe et al animal model, periodontitis is of bacterial origin 1970s Consensus of bacterial infection www.indiandentalacademy.com
  • 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 as the pathogen causing Aggressive Periodontitis www.indiandentalacademy.com
  • 15. Etiologic agents Haffajee & Socransky 1994 www.indiandentalacademy.com
  • 16. Periodontitis : A sequential infection? (Williams et al 1985) Species A causes disease Mounts a host response Arrest of progression Suppression below disease causing levels Recurrence of disease with species B Repetition of cascade Numerous antibodies to antigens www.indiandentalacademy.com
  • 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. www.indiandentalacademy.com
  • 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 issue B) 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 www.indiandentalacademy.com
  • 20. Microbial testing Repeat Microbial testing www.indiandentalacademy.com
  • 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. www.indiandentalacademy.com
  • 22. Bacterial infections release of inflammatory cells (PMNls etc) Triggering of viral infctions Viruses reside in the inflammatory cells Treat the bacterial infection Diminished viral counts Reduced inflammatory cells www.indiandentalacademy.com
  • 23. Pathogenesis : 1960s : focus on the bacterial effect on the host 1970s : focus on the host factor Ivanyi and Lehner 1970 peripheral blood mononuclear cells sensitised to antigens of infecting bacteria Lavine 1976 discovery of defective neutrophils (less chemoattractant reaction) Mediators Of Inflammatory Response PGs, cytokines , chemokines (Stolman J, Maderazo 1976) MMPs (Reynolds) www.indiandentalacademy.com
  • 24. Pathways : Normal individual Plaque accumulation Chemoattarctants like IL-8 produced (vascular inflammation) E-selectin Neutrophil binding www.indiandentalacademy.com
  • 25. Primary host CR3 defens e Susceptible individuals macrophages take over www.indiandentalacademy.com
  • 26. Disease Health IL-1beta, TNF-alpha, TNF-gamma,PGE2 ,MMPs high low IL-4,IL-10,TGF-beta,IL-1ra,TIMPs low high www.indiandentalacademy.com
  • 27. Environmental and acquired risk factors Cytokns prostnoids PMns Antbdy Host Connective Clinical signs Microbial Immuno Tissue and of disease challenge Inflammatory MMPs host & antigns response metabolism progression LPS Genetic risk factors KORNMAN & LOESCHE 1997 www.indiandentalacademy.com
  • 29. Susceptibility : Genetic based and Risk based Genetic factors : Susceptibility : variation in normal genetic sequences e.g. polymorphism in the gene encoding for IL-1alpha, beta … increased severity of the disease. EOP : possible genetic risk factor www.indiandentalacademy.com
  • 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 www.indiandentalacademy.com
  • 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 www.indiandentalacademy.com
  • 32. Diagnosis : Until 1980s… LJP & Chronic Marginal Periodontitis Periodontitis : homogenous disease Family of closely related diseases with differing natural histories, responses to therapy and prognoses. 1983 1989 1999 www.indiandentalacademy.com
  • 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 as a class of agents causing illness, is mistaken and misleading for several good reasons: many diseases remain of unknown cause; known causes are of diverse types; causation may be complex, with interplay of several factors, intrinsic; and, more generally, an effect – the disease – should not be confused with its own cause’. Scadding www.indiandentalacademy.com
  • 34. “ …The names of diseases are a convenient way of stating briefly the endpoint of a diagnostic process that progresses from assessment of symptoms and signs towards knowledge of causation.” Scadding Set of criteria : if fulfilled …. Come to a diagnosis. Periodontitis : more of a syndrome than a disease Complex etiology and a cluster of signs & symptoms van der Velden 2005 www.indiandentalacademy.com
  • 35. Classification of pdl disease in exhaustive and exclusive way. Based on age Based on extent of the disease ( number of teeth affected ) Based on severity ( CAL and PD) Based on clinical characteristics van der Velden 2000 www.indiandentalacademy.com
  • 36. Radiographs : Standard recommendation for initial examination of a periodontitis patient 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 based radiography Aim : detect hard tissue changes but… using underexposed, serial radiograph with CADIA may reveal supracrestal soft tissue changes www.indiandentalacademy.com
  • 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 www.indiandentalacademy.com
  • 38. Normative reference value for a disease temperature > 37.7°c… fever Normal Periodontium : Strictly no pockets above 3mm arbitrary values and define periodontal pockets www.indiandentalacademy.com
  • 39. NHANES III 28 year old : 2 pockets > 5mm –destructive PDL disease 58 year old: 5 pockets > 5mm www.indiandentalacademy.com
  • 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 www.indiandentalacademy.com
  • 41. Assessment of Risk factors in Diagnosis. 1980s When 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 www.indiandentalacademy.com
  • 42. Risk Factors : www.indiandentalacademy.com
  • 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 www.indiandentalacademy.com
  • 44. Systemic diseases predisposed for periodontal disease : Vice versa : Pdl disease predisposing to systemic diseases. DeStefano et al 1993 9760 subjects 14 years 25 % increased risk for developing CHD www.indiandentalacademy.com
  • 45. Issues in therapy 1960s Surgical 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 www.indiandentalacademy.com
  • 46. 1980s Guided 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 www.indiandentalacademy.com
  • 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 www.indiandentalacademy.com
  • 48. non-responding patients : unable mount an immune response. Perrson et al 1994 macaca fascicularis injected with a dead bacterial strain Cessation of alveolar bone loss Pharmacotherapy in periodontics LDD : delivery of the drug at high concentration for longer periods directly to the pockets Antibiotics as adjuncts to mechanical therapy (empirical) www.indiandentalacademy.com
  • 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 www.indiandentalacademy.com
  • 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. www.indiandentalacademy.com