AGGRESSIVE PERIODONTITIS NIDHI B.D.S FINAL YEAR
CONTENTS • Introduction • History • Aggressive periodontitis • Difference between chronic and aggressive periodontitis • Clinical features • Localized aggressive periodontitis • Generalized aggressive periodontitis • Difference between LAP & GAP • Risk factors • Microbiologic factors • Immunologic factors • Genetic factors • Environmental factors • Conclusion • references
INTRODUCTION • Periodontitis is defined as an inflammatory disease of the supporting tissue of the teeth caused by specific microorganisms, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession, or both.
HISTORY • 1923, Gottlieb -- Case of epidemic influenza • “Diffuse atrophy of the alveolar bone” • Loss of collagen fibers in the periodontal ligament • Replacement by loose connective tissue • Extensive bone resorption, • Resulting in a widened periodontal ligament space. • The gingiva apparently was not involved.
In 1938 Wannenmacher described incisor-first molar involvement and called the disease Parodontitis marginalis progressiva. • Finally in 1967, Chaput and colleagues and by Butler in 1969 introduce the term Juvenile Peridontitis. • In 1989 the World Workshop in Clinical Periodontics categorized this disease as ‘Localized Juvenile Periodontitis’ (LJP) • Most recently , it is named as Aggressive Periodontitis.
Aggressive periodontitis • Aggressive periodontitis (AgP) comprises a group of rare, often severe, rapidly progressive forms of periodontitis often characterized by an early age of clinical manifestation and a distinctive tendency for cases to aggregate in families. (Clinical Periodontology and Implant Dentistry 4th edition)
Aggressive periodontitis describes three of the formerly classified as “early-onset periodontitis” They are: • Localized aggressive periodontitis • Generalized aggressive periodontitis • Rapidly progressive periodontitis
Features of aggressive periodontitis (by lang et al. in 1999) PRIMARY FEATURES • Non contributory medical history • Rapid attachment loss and bone loss • Familial aggregation
SECONDARY FEATURES • Amount of microbial deposits does not commensurate with the severity of periodontal tissue destruction • Elevated proportions of aggregatibacteractinomycetemcomitans (Aa) • Hyper responsive macrophage phenotype with exaggerated response to bacterial endotoxin • Phagocyte abnormalities
Localized aggressive periodontitis • Clinically, it is characterized as having "localized first molar/incisor presentation with interproximal attachment loss on at least two permanent teeth, one of which is a first molar, and involving no more than two teeth other than first molars and incisors” .
Clinical features: • Age of onset at about puberty. • Affects both the sexes • Main characteristic feature affects mainly the FIRST MOLARSandINCISORS • Lack of clinical inflammation despite the presence of deep periodontal pockets.
Plaque that is present forms thin biofilm on the teeth. • Plaque contains elevated levels of :Aggregatibacteractinomycetem-comitans (Serotype b)Porphyromonasgingivalis (in some pts) • Disease progresses rapidly and Plaque that is present forms a thin biofilm on the teeth and rarely mineralizes to form calculus
The rate of bone loss is 3 to 4 timesfaster than in chronic periodontitis. • Robust serum antibody response. to infecting agents
Other Clinical Findings: • Maxillary incisors migrate disto-labially that results in diastema formation. • Increasing mobility of the affected teeth • Sensitivity of denuded root surfaces to thermal and tactile stimuli • Deep, dull radiating pain during mastication. • Periodontal abscess may form. • Regional lymph node enlargement may occur.
Radiographic finding: • Classic diagnostic sign VERTICAL LOSS of alveolar bone around the first molars and incisors. • Other finding “Arc-shaped” loss of alveolar bone extending from the distal surface of 2nd premolar to the mesial surface of the 2nd molar. • Bone defects are usually wider than usually seen with chronic periodontitis.
Generalized aggressive periodontitis “Characterized by generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors”
FEATURES • Usually affecting persons under 30 years of age, but patients may be older. • Poor serum antibody response to infecting agents. • Generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors. • Pronounced episodic nature of the destruction of attachment and alveolar bone.
Radiographic features • No definitive pattern of distribution. Ranges from severe bone loss associated with the minimal no. of teeth, to advanced bone loss affecting the majority of teeth in the dentition. • Patients with GAP demonstrate osseous destruction of 25% to 60% during a 9 week period and other sites show no bone loss.
Risk factors for aggressive form of periodontitis • Microbiologic factors • Immunologic factors • Genetic factors • Environmental factors
Microbiologic factors • Presence of Aggregatibacteractinomycetemcomitans (Aa) is a key agent in LAP as it is present in high nos. & the patient has high titre of serum antibodies against Aa. • Virulence factors possessed by Aa, such as leucotoxin, lipopolysaccharide, proteases, collagenases, surface associated material affect the immune response & lead to connective tissue destruction and bone resorption.
Immunologic factors • Defective chemotaxis due to functional defect of PMNs. • Hyper responsive monocytes that increase prostaglandin, IL-1 α IL-1βproduction, which result in one resorption. • Human leucocyte antigen (HLA) A9 & B 15 are recognized as candidate markers of aggressive periodontitis.
Genetic factors • Tendency to occur in families: familial aggregation • Segregation & linkage analysis have shown that presence of specific gene is responsible for neutrophil abnormalities • Transmission through autosomal- dominant mode of inheritance
Environmental factors Smoking has a significant influence in the progression of generalized aggressive periodontitis. Smokers have greater attachment loss than non smokers.
CONCLUSION • Aggressive forms of periodontitis are currently considered to be multifactorial diseases developing as a result of complex interactions between specific host genes and the environment. • Interactions between the disease process and environmental factors and genetically controlled modifying factors are thought to contribute to determining the specific clinical manifestation of the disease. • For a successful treatment outcome the conventional therapy is to be combined with a wide range of therapeutic procedures to increase the chances of disease resolution.
REFERENCES • CARRANZA’S CLINICAL PERIODONTOLOGY; 10thedition. • J LINDHE; CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY: 4th edition