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1. Introduction 2.Classification and clinical syndrome 3. Localized aggressive periodontitis 4. Generalized aggressive periodontitis 5. Epidemiology - primary and permanent dentition 6. Risk factors for periodontitis 7. Etiology and pathogenesis - Microbiological factor - Immunological factors - genetic factor - Environmental factor - Current concept 8. Diagnosis 9.Treatment
Chronic
Aggressive
Necrotising
SECONDARY FEATURES
Hyperresponsive macrophage phenotype, including elevated PGE2 and IL1 in response to bacterial endotoxins
Phagocyte abnormality
Mombelli et al 2002
periodontosis
stages -1,2 and 3 HISTORICAL BACKGROUND
In 1928, Gottlieb deep cementopathia and hypothesized that this was a disease of eruption
In 1952 Glickman extreme variant of destructive processes In 1989 the world workshop -of early-onset periodontitis
Historical background
HISTORICAL BACKGROUND
juvenile periodontitis was introduced by Chaput and colleagues in 1967 and by Butler in 1969.
Radiographic features
producing ability
A defect in cementum formation
adolescent population is estimated less than 1%. Most report suggest a low prevalence about 0.2%
particularly in the youngest age group whereas other report no male female differences in incidence. Among blacks, males are affected more than females.
Radiographic findings
minimal number of teeth, to
advanced bone loss Vertical loss of alveolar bone Arc shaped loss of alveolar bone
Epidemiology
Epidemiological studies relate aggressive periodontitis to
showing up to 51.5 % affected individuals. These differences are probably due to the difference in the employed epidemiological methodologies definition of early onset periodontitis
PRIMARY DENTITION
Little evidence is available few studies marginal alveolar bone loss
necessarily mean presence of an aggravated form of periodontitis, abundance of local factors( plaque and calculus).
but may indicate a chronic form of disease with relative tooth exfoliation early in life are usually interpreted as
Permanent dentition
In permanent dentition between age group between 3-20
year prevalence of periodontitis is less than 1%.however it differs among different population: In US school children 5-17 yrs prevalence is 0.2% for whites, 2.6% for blacks ( Loe & Brown) Longitudinal studies have shown that young age subjects with signs of destructive periodontitis are prone to further deterioration. -more pronounced - initially affected sites, patient diagnosed with LAP and low socioeconomic states. -involves both an increase in extent and increase in severity of lesion.( Clerehugh et al 1990, Lissau et al 1990, Albander et al 1991a,b, 1993, Aass et al 1994)
Risk factors
Microbiological Immunological Genetic Environmental Current concept
Bacterial etiology
AAc
Campylobactor rectus
Capnocytophaga species Eikenella coorrodens Prevotella intermedia
Bacterial etiology
Eikenella corrodens
Prevotella intermedia
campylobactor
capnocytophaga
AAC
marginal periodontium via two related mechanism 1. Direct action of the microorganism or their products on the host tissue 2. As a result of their eliciting tissue damaging inflammatory response
Host defense
Intact epithelial barrier Salivary components Sulcular fluid components local antibody production high level of tissue turnover presence of normal flora or
disease Demonstration of the virulence factor including leucotoxin Finding of immune response correlation between treatment outcome and level of AAC
Leucotoxin
Endotoxin
Virulence factors
Collagenase
bacteriocin
B cell and antibody producing plasma cell (Lijenberg & Lindhe 1980)
Type of Plasma cell.( Mackler et al 1977,1978) Depressed T-helper to T- suppressor ratio in blood
LAP
PMNs abnormality -result of a hyper -inflammatory state - pro-inflammatory cytokines (Shapira et al 1994, Agarwal et al 1996).
Genetic factor
prevalence of AgP is high among certain famlies whearas percentage of affected sibling may reach 40-50%. pattern of disease transmission is consistent with mendelian inheritace of a gene of major effect. This means that observed familial pattern can be partly accounted for by one or more genes that could predispose individual to develop AgP.
Genetic factors..
Segregation analysis - Autosomal dominant It is possible to find other mode of inheritance in different
population. Linkage analysis - chromosomal location of a gene of major effect for a trait. Several loci have been proposed as genes conferring increased susceptibility to AgP. these genes are associated with neutrophils function and with the host ability to effectively deal with the LPS exposure.
Genetic factors..
Beside gene of major effect other gene may act as
modifying gene The ability to control high titer of specific antibodies is race dependent and probably protective. Allelic variation in the Fc receptor for IgG2 immunoglobulin have also been suggested to play role in suboptimal handling of Aac infection. PMNs expressing the R131allotype of FcRIIa( Fc receptor containing an arginine instead of histidine at amino acid 131) shows decreased phagocytosis of A.a.
Segregation analysis
Aggressive periodontitis aggregates in families. suggests but does not prove the disease has a genetic basis
because .
in the same family, the probability of two rare disease occurring in same family is exceedingly small.
juvenile periodontitis) have been observed in the same family and found to occur sequentially in the same individual. These findings suggest there are common genetic risk factor for the subforms of AP.
Segregation analysis..
Many reports in the literature describing families with
multiple effected individuals Pattern of disease in these families lead to investigation Both dominant and recessive mode of inheritance for AP disease
probands were not consistently unaffected) U.S. study conducted African-american and Caucasian families - Autosomal dominant
Despite inconsistent conclusion regarding their mode of inheritance, segregation analysis consistently have supported the role of major gene in the etiology of AP.
Schenkein
MODEL OF INHERITANCE
Linkage studies
Linkage between the AgP and a specific chromosomal
region. (Boughmen et al first reported) Autosomal dominant form of AgP & dentinogenesis imperfecta (DGI). AgP disease gene - long arm of chromosome 4 near the gene for DGI. Aggressive periodontitis does not typically co-segregate with DGI, however, and it is unlikely an important AP disease gene reside within this chromosomal region in the more general population.
Association studies
Role of HLA
More than 40 autoimmune diseases are associated with
HLA antigen. Two antigens HLA A9 and HLA B15. The risk of disease in subjects wit HLA A-9 and B-15 is about 1.5 to 3.5 times greater . HLA-A2 antigens - less prevalent in AgP patients (may be protective.
ASSOCIATION STUDIES
Class II DR4 antigen - association with type I diabetes
mellitus. DR4 antigen - is more prevalent in AgP patients in control, (Katz et al ). Role of IL-1 Pleiotropic; stimulate bone resorption , inhibit collagen synthesis, and up-regulate matrix metalloproteinase activity and prostaglandin synthesis. Polymorphism in the vitamin-D receptor and IL-1 receptor antagonist genes and mutation in the N-formyl-1-methionyl-1-leucyl-1phenylalanine receptor gene have been associated with aggressive periodontal disease.
molecule)
Actalasia
Chronic and cyclic neutropenia Chediak Higashi syndrome
Catalase enzyme
Unknown abnormal transport of vesicle to and
from neutrophils lysosomes caused by mutation in the lysosome trafficking regulator gene.
unknown for EDS type VIII
continue
DISORDER
Papillon lefevre syndrome Hypophosphatasia Trisomy 21 Prepubertal-
PROTEIN/TISSUE DEFECT
Catepsin C dipeptidyl
aminopeptidase I
Tissue nonspecific alkaline
phosphatase
Multiple; critical trisomic region
at least 5 Mb long
periodontitis(non syndromic)
Kindler syndrome
Cathepsin C
Immunologic factors
Role of immune defect - pathogenesis of AgP Role of HLA - HLA A9 and B15 antigens
Monocytes or both. can impair either the chemo tactic attraction / phagocytosis AAC as well as some strains of most putative periodontal pathogens are resistant to serum mediated killing mechanisms.
Immune defect..
Deficiency in GP110
Immunological factor
The molecular basis for the receptor defect is postulated to be inherited as an intrinsic cellular defect
or a modulation of neutrophils receptor expression by elevated level of proinflammatory cytokines including IL-1 and TNF
LAP patients who do not show G-protein couple receptor deficiency has the same clinical feature as with the neutrophils defect. This suggests that the G-protein couple receptor deficiency is sufficient but not essentially for LAP, and other alteration of the host bacterial interaction may yield a similar clinical outcome
Immunological factor.
In LAP collagenase (in tissues & GCF) MMP-1 TIMP-1 Elevated level of antibodies to AAC ( IgG2)
immunological factor.
variant of the Fc receptor on neutrophils ( R131 allele of FcRII-)
does not efficiently bind IgG2
B/C of less efficient binding , an antibody response more vigorous than normal is necessary to control the AAC infection in LAP,
supported by the observation that patient with an elevated antibody response have significantly less loss of attachment.
In comparison, individual with generalized early onset periodontitis do not develop a strong antibody response which support the hypothesis that antibodies function to limit the disease process.
Endotoxin from AAC can induce Schwartzman reaction, macrophage toxicity, platelet aggregation, complement activation and bone resorption
Polyclonal Blymphocytes activation by periodontal bacteria may result in production of antibodies unrelated to the activating agent.
Environmental factors
smoker patients
IgG2
antibody level against A.a. significantly depressed.
Current concepts
MICROBIAL EXPOSURE & INFECTION ,AAC NORMAL LAP CIGGRETTE SMOKING P.GINGIVALIS & OTHER BACTERIA GAP
GENETIC PREDISPOSITION
GENE OF MAJOR EFFECT AUTOSOMAL DOMINANT INHERITANCE
GENETIC MODIFYING FACTORS IgG2 RESPONSE AGAINST AAC, IMMUNOGLOBULIN RESONSE AGAINST OTHER BACTERIA
Diagnosis
CLINICAL
MICROBIOLOGIC
GENETIC
Clinical diagnosis
clinical examination, medical and dental history
more advanced aids are to properly diagnose, treatment plan and monitor the disease.
QUESTIONS TO BE ANSWERED
is there periodontitis is there loss of periodontal support is there a plausible cause for attachment loss other than periodontitis
.
Is there process imitating periodontal disease by pseudo pocket formation. recognize different causes for the attachment loss must rule out other causes attachment loss
.
clinical diagnosis.
The question here is does the patient have a systemic condition medical history is fundamental
differential diagnosis between LAP and GAP exclusion of the presence of modifying factors/ contributory factors such as smoking and drug abuse
Microbiologic diagnosis
presence of AAC - secondary feature of AgP. successful treatment of LAP depends on
performed, microbiologic testing may be postponed until the first phase is completed.
Microbiological diagnosis
But the reduction in the bacterial load -false negative result
suppression of AAC.
microbial testing of spouse, children or siblings of AgP
bacterial pathogens AgP patients have higher level of PGE2 in GCF( indicating that monocytes from these patients respond to bacterial and inflammatory stimuli with very high level of local release of inflammatory mediators). These may induce an exuberant reaction associated with high level of activation of tissue degrading matrixmetalloproteinases.
trait.
Some of the LAP cases may progress to GAP, so early
detection of patients infected with Actinobacillus actinomycetemcomitans producing low level of specific antibodies may indicate early identification of high risk group for GAP.
Genetic diagnosis
Evaluation of siblings of the probands
and other family members should be done. construction of a pedigree of the AgP trait. Such diagnosis may bring considerable information regarding the level of risk shared with the family and helps to establish the need for monitoring clinically unaffected individuals.
All the evidences gathered during
Therapeutic modalities
Early detection.
initial diagnosis-radiographs to assess the rate of progression of the disease. future radiographs - facilitate the clinician assesment of treatment success and control of the disease.
therepeutic modalities.
Educate the patient about the disease & family members therapeutic considerations
-control the infection, -arrest the disease progression, -correct anatomic defects, replace the missing tooth
therapeutic modalities.
Conventional periodontal therapy Surgical resective therapy Regenerative therapy Antimicrobial therapy Microbial testing Local delievery Host modulation Treatment planning and restorative consideration
Outcome Assessment
1. Significant reduction of clinical signs of gingival
inflammation; 2. Reduction of probing depths; 3. Stabilization or gain of clinical attachment; 4. Radiographic evidence of resolution of osseous lesions; 5. Progress toward occlusal stability; 6. Progress toward the reduction of clinically detectable plaque to a level compatible with periodontal health.
conclusion