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Presented by: Dr. Krishna Das 1st Yr PG Student Department of Periodontology and Oral Implantology
Aggressive Periodontitis
Aggressive periodontitis, by definition, causes rapid destruction of the periodontal attachment apparatus and the supporting alveolar bone.
Aggressive periodontitis may be further classified into: 1) Localized Aggressive Periodontitis 2) Generalized Aggressive Periodontitis
Aggressive Periodontitis
The following characteristics are common to patients with aggressive periodontitis:
The following characteristics are common but not universal: Diseased sites infected with Actinobacillus actinomycetemcomitans (now Aggregatibacter actinomycetemcomitans, A.a.) Abnormalities in phagocyte function. Hyperresponsive macrophages, producing increased prostaglandin E2 (PGE2) and interleukin-1 (IL-1). In some cases, self-arresting disease progression.
Historical Background
In 1923, Gottlieb
In
called diffuse atrophy of the alveolar bone and deep cementopathia. 1938, Wannenmacher described incisor-first molar involvement and called the disease parodontitis marginalis progressiva. the concept of periodontosis as a degenerative entity was unsubstantiated and that the term should be eliminated from periodontal nomenclature. term juvenile periodontitis was introduced by Chaput and colleagues in 1967 and by Butler in 1969.
The
In
1971, Baer defined it as "a disease of the periodontium occurring in an otherwise healthy adolescent which is characterized by a rapid loss of alveolar bone about more than one tooth of the permanent dentition. The amount of destruction manifested is not commensurate with the amount of local irritants."
In
1989 the World Workshop in Clinical Periodontics categorized this disease as localized juvenile periodontitis (LJP), a subset of the broad classification of early onset periodontitis (EOP).
Minimal plaque that rarely mineralizes. However Maxillary incisors migrate in distolabial
direction diastema.
Increasing mobility of affected teeth. Sensitivity of denuded root surfaces. Periodontal abscess formation.
Localized aggressive periodontitis in 17-year-old girl. Gingival inflammation, periodontal pockets, and pathologic migration.
Following initial attack, host responds and produces antibodies which improve phagocytosis of bacteria and neutralize leucotoxic activity
Additional reasons: #2: A.a. may lose its ability to produce leukotoxin. This may
slow or arrest the disease process.
Radiographic Evaluation
Vertical bone loss occurs ,usually bilateral, affecting first permanent molars & incisors. Arc-shaped bone loss extending from the distal surface of the 2nd premolar to the mesial surface of the 2st molar.
Clinical and cone beam CT view of advanced alveolar bone resorption around incisors and first molar in a 24-year-old male with aggressive periodontitis.
Usually affects persons 30 years & younger but can affect older
persons.
Often plaque is minimal but contains high levels of: A.actinomycetemcomitans P..gingivalis Tannerella forsythia (previously B. forsythus)
Destructive phase:
Non-destructive phase:
Tissues may appear pink with some stippling Lack of inflammation Probing will reveal deep pockets Bone & attachment levels relatively stable
Some clients with GAP may exhibit: Weight loss Mental depression general malaise Systemic conditions may predispose patient to GAP, these include chronic neutrophil defects, leukocyte adherence deficiency Functional defects of PMNs, monocytes or both
Radiographic Evaluation
to
Generalized aggressive periodontitis and poor crown-to-root ratio in 24year-old patient; overall prognosis poor. A, generalized periodontal attachment loss and pocket formation. B, Moderate to advanced bone destruction. The contrast between the well-formed crowns and the relatively short, tapered roots worsens the prognosis.
Risk Factors
1) Microbiologic Factors
A.a. has been implicated as the primary pathogen associated with LAP. A.a. produces a strong leukotoxin kills neutrophils.
Different strains of A.a. produce different levels of leukotoxin: Highly toxic strains produce greater numbers of leukotoxin People with the disease more likely to have highly toxic strains (African-Americans in particular)
2) Immunologic Factors
The human leukocyte antigens (HLAs), which regulate immune responses, have been evaluated as candidate markers for aggressive periodontitis( HLA A9 and B15 )
Functional defect in PMNs and monocytes or both: -Impaired chemotaxis -Impaired phagocytosis
PGE2
receptor for human immunoglobulin G2 (IgG2) antibodies, have been shown to be disproportionately present in patients with LAP. Autoimmunity has a role in GAP collagen, DNA and IgG.
host antibodies to
3) Genetic Factors All individuals are not equally susceptible to aggressive periodontitis. Familial pattern of alveolar bone loss
Data support the concept that a gene or genes of major effect exists
for aggressive periodontitis.
Data
also support a genetic basis for some of the immunologic defects seen in patients with aggressive periodontitis.
However,
it is unlikely that all patients affected with aggressive periodontitis have the same genetic defect.
4) Environmental Factors
The amount and duration of smoking are important variables that can influence the extent of destruction seen in young adults. Patients with GAP who smoke have more affected teeth and more loss of clinical attachment than nonsmoking patients with GAP. However, smoking may not have the same impact on attachment levels in younger patients with LAP.
whether the disease is generalized or localized, the degree of destruction present at the time of diagnosis, and the ability to control future progression.
Therapeutic Modalities
Early detection : preventing further destruction more
predictable than attempting to regenerate lost supporting tissues.
Surgical Therapy:
1) Resective Therapy: decreases or eliminate pocket depth. Limitations: Further risk of increased mobility. careful evaluation of risk/benefit must be considered from case to case
2) Regenerative Therapy: bone grafts, barrier membrane and wound healing agents. In intrabony defect particularly vertical with multiple walls.
Limitations: -patients with severe bone loss -depends on anatomy of defect and tooth involved.
1) Systemic Antibiotics: -more favorable clinical response -increase in clinical attachment level -decrease probing pocket depth -decrease risk of additional attachment loss antibiotics used: amoxicillin tetracycline amoxicillin + metronidazole clindamycin doxycycline 2) Microbial testing: Advocated by some clinician for sensitivity and resistance to select antibiotics. But according to Carranza empirical use of antibiotic (amoxicillin and metronidazole) is more clinically sound and cost effective. 3) Local drug delivery: for localized infections. advantages: -small total dose -avoid systemic side effects - exposure to target microorganism to high concentration so more therapeutic level of medication is achieved
Also causes: Reduced cytokene level Stimulates osteoblastic activity New bone formation by upregulating collagen production
Restorative considerations:
Sever teeth should be extracted -outcome of treatment limited -their retention may cause additional bone loss Restoration of lost tooth: 1) Transplantation: have been attempted but with limited success. 2) Dental Implants: recent studies (eg. Mengel et al.) have shown successful implant rehabilitation for partially edentulous in patient with treated for GAP. But it was observed that the bone loss and attachment loss around implant patient in GAP > periodontally healthy patient.
Distribution
Antibody response
Racial predilection
Familial Tendency Gender distribution PMN/ Macrophage Defect
No
Yes ? Yes
Some cases
Variable
Yes
Good