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

Critical Issues In Periodontal
Research

INDIAN DENTAL ACADEMY
Leader in Continuing Dental Education

www.indiandentalacademy.com

Introduction


Epidemiology and Prevalence :

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


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 )


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 )


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


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)


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


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


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


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


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


Etiologic
agents

Haffajee & Socransky 1994


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


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.

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


Microbial
testing

Repeat
Microbial
testing


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.


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


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)

Pathways :
Normal individual

Plaque accumulation

Chemoattarctants like IL-8 produced
(vascular inflammation)

E-selectin

Neutrophil binding


Primary
host
CR3
defens
e

Susceptible individuals
macrophages take over

Disease Health
IL-1beta, TNF-alpha,
TNF-gamma,PGE2 ,MMPs
high low

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


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

, Birkadel-Hansen1993


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


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


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


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


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


“ …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


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


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


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


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

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


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


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


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


Risk Factors :


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


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


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


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


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


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)


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


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.


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

Empfohlen

Empfohlen

Weitere ähnliche Inhalte

Was ist angesagt?

Was ist angesagt? (19)

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

Ähnlich wie Critical issues in periodontal research /certified fixed orthodontic courses by Indian dental academy (20)

Mehr von Indian dental academy

Mehr von Indian dental academy (20)

Kürzlich hochgeladen

Kürzlich hochgeladen (20)

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