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Aggressive Periodontitis: a Review www.djas.co.in REVIEW ARTICLE ISSN No-2321-1482 DJAS 1(III), 129-135, 2013 Dental JOURNAL All rights are reserved of A d v a n c e S t u d i e s AGGRESSIVE PERIODONTITIS: A REVIEW Dr. Baljeet Singh1 Dr. Avnika Garg2 Dr. Rahul K. Garg3 1Prof. & Head Department of Periodontics, Bhojia Dental College and Hospital, Distt. Solan, Himachal Pradesh (India) 2PG Student Department of Periodontics, Bhojia Dental College and Hospital, Distt. Solan, Himachal Pradesh (India) 3MBBS, MBA (IIM Ahmadabad) (India) Corresponding Author: 1Mobile: 919814510711 Email: [email protected] ABSTRACT Received : th 10 June, 2013 Aggressive periodontitis, which encompasses a number of clinical entities, probably results from the mobilization of tissue‟s destructive mechanisms which are common to most forms of periodontal diseases. The unique attributes Accepted: of the disease process are due to the virulence of the pathogens and the host susceptibility may be due to the th 27 August, 2013 heritable or acquired susceptibility factors, which permit expression of periodontitis at a relatively younger age. Available online: Keywords: Periodontitis, Aggressive Periodontitis, Periodontal diseases. th 28 Dec, 2013 INTRODUCTION PRE-PUBERTAL PERIODONTITIS (PPP) Severe, rapid periodontal destruction and tooth loss Periodontitis is defined as “an inflammatory disease occur infrequently in children and teenagers and can of the supporting tissues of the teeth caused by be classified in two groups according to the age of specific microorganisms or group of specific onset: prepubertal forms, which occur before 11 microorganisms, resulting in progressive destruction years of age, although they may extend beyond this of the periodontal ligament and alveolar bone with period, and the pubertal and adolescent forms, which are seen approximately between 11 and 19 years of pocket formation, recession or both.1 Aggressive age. The term juvenile periodontitis is used to refer to periodontitis may be universally distinguished from the second group. Both prepubertal and pubertal chronic periodontitis by the age of onset, the rapid forms have been sub-classified into localized and rate of disease progression, the nature and generalized forms, depending on their distribution in composition of the associated sub gingival micro the mouth.6 This is an extremely rare form of flora, alterations in the host‟s immune response, and periodontal disease characterized by rapid a familial aggregation of diseased individuals.2 In periodontal destruction of the primary dentition.4 The addition, a strong racial influence is observed in the disease begins about the age of 4 years or before, during or immediately after eruption of the primary United States; the disease is more prevalent among 7 African Americans.3 Aggressive periodontitis teeth, but may affect the permanent dentition. Primary teeth are lost by the age of 5 or 6 years. The describes three of the diseases formerly classified as 1 permanent teeth then erupt normally but within few “early-onset periodontitis (EOP).” EOP can be years destructive periodontal disease affects all the practically divided into three groups; prepubertal teeth except the third molars. By the age of 15 most periodontitis, juvenile periodontitis and rapidly of the permanent teeth are lost.8 An extremely acute progressive periodontitis.4 Incidental attachment loss inflammation and proliferation of the gingival tissues, is a term used only in epidemiological studies to with rapid destruction of bone, are found.9 In many describe severe destructive lesions which affect instances there is a familial pattern to the disease, and isolated teeth without meeting the criteria for other most if not all cases are probably genetically 4 forms of EOP. This category includes attachment loss mediated. There is tendency for the disease to be adjacent to an impacted third molar.5 refractory to antibiotic therapy, frequent respiratory infections and destruction of the roots of teeth. 129 Dental Journal of Advance Studies Vol. 1 Issue III-2013 Normally children do not present with alveolar bone more sites. Since RPP does not have any resorption characteristic of periodontitis. They may at characteristic diagnostic feature, only periodic the most, have gingivitis especially during puberty.8 evaluation of the rate of tissue destruction will help in In PP, there is an abnormality in chemotaxis of either proper diagnosis.8 blood neutrophils or monocytes or both, resulting from an inability of these cells to adhere to surfaces. LOCALIZED AGGRESSIVE PERIODONTITIS Histological features of generalized PP show an (LAP) absence of neutrophils from the gingiva, but a dense (Localized Juvenile Periodontitis/ Deep lymphoid cell infiltrate consisting of plasma cells is Cementopathia/ Parontitis marginalis progressive/ present in the connective tissue. Thus, extensive bone Familial juvenile periodontitis/Idiopathic Juvenile loss may occur in the absence of neutrophils.7 The Periodontitis/ Periodontosis) flora inhabiting pockets of individual with prepubertal periodontitis has not been studied nor Historical Background have serum antibody titers been determined.10 In 1923, Bernard Gottlieb reported a patient with a fatal case of epidemic influenza and a disease that he RAPIDLY PROGRESSIVE PERIODONTITIS called “diffuse atrophy of the alveolar bone.”11 In (RPP) 1928, he attributed this condition to the inhibition of Rapidly progressive periodontitis (RPP) is continuous cementum formation, which he characterized by severe generalized periodontal considered essential for maintenance of the PDL destruction, and may affect any or all of the fibers. He then termed the disease “deep permanent dentition of patients between the ages of cementopathia” and hypothesized that this was a 20 and 35 years. On present available evidence it is “disease of eruption” and that cementum initiated a difficult to justify the classification of this condition foreign body response.12 In 1938, Wannenmacher as a separate disease entity, as it could well represent described incisor–first molar involvement and called a rapidly progressive chronic periodontitis in a the disease “parodontitis marginalis progressiva.”1 susceptible individual. It is also important to Contrary to others at that time, Wannenmacher distinguish this condition from post-juvenile considered this disease an inflammatory process.9 periodontitis, and to remember that some conditions, Several explanations evolved for the etiology and such as Down's syndrome, have a high susceptibility pathogenesis of this type of disease.13 In 1940, to severe rapidly progressive periodontitis in the Thoma and Goldman used the term “paradontosis” to permanent dentition.4 refer to this disease; the initial abnormality was located in the alveolar bone rather than in the It may be associated with systemic disease and be cementum and consisted of vascular resorption and refractory to all forms of therapy. Most patients with halisteresis rather than “lacunar resorption”. In 1947, RP demonstrate abnormalities in peripheral blood Goldman described vascular resorption and neutrophil function that are manifested in an impaired halisteresis in a spider monkey as being due to a chemotactic ability.7 Distribution of lesions does not degenerative non-inflammatory disease of the show any definite pattern. It may be localized to few supporting structures. In 1942, Orban and Weinmann teeth or may be generalized.8 The features of RPP introduced the term “periodontosis” and, on the basis include an active phase of severe, rapid bone of one autopsy case studied in detail, described the destruction involving most of the teeth; spontaneous development of the disease. Most of the above or rapid slow-down of the process; proliferation and mentioned studies considered “periodontosis” a severe inflammatory response during active phase; degenerative disease caused by unknown systemic functional defects in neutrophils or monocytes in the factors. Glickman in 1952 believed that the majority of affected patients; the possibility of conditions described in these studies didn‟t represent previous juvenile periodontitis; and systemic a different type of periodontal disease, but rather disturbances that may include weight loss, mental extreme variants of destructive processes common to depression and general malaise. Treatment consisting all periodontal disease.9 Other investigators denied of root planing and antibiotic therapy is generally the existence of a degenerative type of periodontal effective.7 Patients with chronic periodontitis may disease and attributed the changes observed to trauma develop rapidly progressive periodontitis in one or from occlusion. Finally, in 1966, the World 130 Dental Journal of Advance Studies Vol. 1 Issue III-2013 Workshop in Periodontics concluded that the concept chemotaxis. Thus leukocytes are prevented of “periodontosis” as a degenerative entity was from reaching the site of infection. unsubstantiated and that the term should be 3. Endotoxin: A.actinomycetemcomitans eliminated from periodontal nomenclature.14 The term releases endotoxin which can induce “juvenile periodontitis” was introduced by Chaput Schwartzman reactions, platelet aggregation, and colleagues in 1967 and by Butler in 1969.15 Baer complement activation and bone resorption. (1971) described juvenile periodontitis as a well- Endotoxin released by Capnocytophaga and defined clinical entity different from adult Bacteroids are weakly toxic but may induce periodontitis in that it appears
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