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Aggressive periodontitis
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- 2. Aggressive periodontitis (formerlyknown as early onset periodontitis) is periodontal destruction that becomes clinically significant around adolescence or early adulthood. It generally affects systemically healthy individuals less than 30 yrs old, although patients may be older. Aggressive periodontitis may be universally distinguished from chronic periodontitis by the age of onset, the rapid rate of disease progression, the nature and composition of the associated subgingival microflora, alterations in the host’s immune response and a familial aggregation of diseased individuals.
- 3. Former classification Present Earlyonset periodontitis Aggressive periodontitis 1) Localized juvenile periodontitis Localized aggressive periodontitis 2) Generalized juvenile periodontitis Generalized 3) Rapidly progressive periodontitis aggressive periodontitis
- 4. Localized aggressive periodontitis: Historical background : In 1923, Gottlieb reported a patient with fatal care of epidemic influenza – “Diffuse atrophy of the alveolar bone”. This disease was characterized by loss of collagen fibers in the periodontal ligament & their replacement by loose connective tissue & extensive bone resorption resulting in widened periodontal ligament space. The gingiva was apparently not involved. In 1928, Gottlieb attributed this condition to the inhibition of continuous cementum formation which was essential for maintenance of periodontal ligament fibers & termed the disease – Deep Cementopathia.
- 5. Gottlieb hypothesized thatdeep cementopathia was a “disease of eruption” & that cementum initiated a foreign body response. As a result it was postulated that the host attempted to exfoliate the tooth resulting in the observed bone resorption & pocket formation. In 1938, Wannenmacher described incisor – first molar involvement & called the disease Parodontitis Marginalis Progressiva. Many individuals considered this to be a degenerative, non inflammatory disease process & because gave it the name Periodontosis. Other investigators attributed the changes observed to trauma from occlusion.
- 6. Ultimately, in1966 the world workshop in periodontics concluded that the concept of periodontosis as a degenerative entity was unsubstantiated & that the term should be removed from periodontal nomenclature. The term Juvenile Periodontitis was introduced by Chaput & colleagues in 1967 & by Butler in 1969. 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.
- 7. In 1989the world workshop in clinical periodontics categorized this disease as localized juvenile periodontitis (LJP). Under this classification system, age of onset & distribution of lesions were of primary importance when making a diagnosis of LJP. Most recently, disease with the characteristics of LJP has been renamed Localized Aggressive Periodontitis.
- 8. Primary features: Clinicallyhealthy Rapid attachment loss and bone destruction Familial aggregation Secondary features : inconsistent amount of microbial deposits, elevated proportions of A.A and P.gingivalis, phagocyte abnormalities, hyper responsive macrophage phenotype, progression of attachment and bone loss may be self arresting.
- 9. Clinical characteristics : Localizedaggressive periodontitis usually has An age of onset around puberty. Robust serum antibody response to invading pathogens. Clinically it is characterized as having “localized first molar / incisor presentation with interproximal attachment loss on atleast two permanent teeth, one of which is first molar, & involving no more than two teeth other than first molars & incisors.
- 10. The followingpossible reasons for the limitation of periodontal destruction to certain teeth have been suggested : 1) After initial colonization of the first permanent teeth to erupt (the first molars & incisors), Actinobacillus actinomycetemcomitans evaded the host defenses by different mechanism including production of polymorphonucleasr leukocyte chemotaxis inhibiting factors, endotoxin, collagenases, leukotoxin & other factors that allow the bacteria to colonize the pocket & initiate the destruction of periodontal tissues. After this initial attack, adequate immune defenses are stimulated to produce opsonic antibodies to enhance the clearance & phagocytosis of invading bacteria & neutralize leukotoxic activity. In this manner, colonization of these sites may be presented. A strong antibody response to infecting agents is one characteristic of localized aggressive periodontitis.
- 11. 2) Bacteria antagonisticto A.actinomycetemcomitans may colonize the periodontal tissues & inhibit A.A from further colonization of periodontal sites in the mouth. This would localize A.A infection & tissue destruction. 3) A.A may loose its leukotoxin producing ability for unknown reasons. If this happens, the progression of the disease may becomes arrested & retarded & colonization of new periodontal sites averted. 4) The possibility that a defect in cementum formation may be responsible for the localization of the lesions has been suggested.
- 12. A strikingfeature of localized aggressive periodontitis is the lack of clinical inflammation despite the presence of deep periodontal pockets. In many cases, the amount of plaque on the affected teeth is minimal, which seems inconsistent with the amount of periodontal destruction present. The plaque that is present forms a thin biofilm on the teeth & rarely mineralizes to form calculus. Although the quantity of plaque may be limited, it often contains elevated levels of A. actinomycetemcomitans & in some patients, Porphyromonas gingivalis. Localized aggressive periodontitis progresses rapidly. Evidence suggests that the rate of bone loss is about 3-4 times faster than in chronic periodontitis.
- 13. Distolabial migrationof maxillary incisors with concomitant diastema formation. Increasing mobility of first molars. Sensitivity of denuded root surface to thermal & tactile stimuli. Deep, dull, radiating pain during mastication, probably because of irritation of the supporting structures by mobile teeth and impacted food. Periodontal abscess may form at this stage and regional lymph node enlargement may occur.
- 14. Radiographic findings : Vertical loss of alveolar bone around the first molars and incisors, beginning around puberty in otherwise healthy teenagers, is a classic diagnostic sign of localized aggressive periodontitis. Radiographic findings may include an “arc-shaped loss of alveolar bone extending from the distal surface of the second premolar to the mesial surface of the second molar”.
- 15. Prevalence and distributionby age and sex : The prevalence of LAP in geographically diverse adolescent populations is estimated to be below 1%. Black males were 2.9 times more likely to have the disease than black females. Several studies have found the highest prevalence of LAP among black males > black females > white females > white males. LAP affects both males & females & is seen most frequently in the period between puberty & 20 yrs of age.
- 16. Generalized aggressive periodontitis: Clinical characteristics : Generalized aggressive periodontitis usually affects individuals under the age of 30, but older patients also may be affected. Poor antibody response to the pathogens present. Clinically characterized by “generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors. The destruction appears to occur episodically with periods of advanced destruction followed by stages of quiescence of variable length (weeks to months or years). Radiographs show bone loss that has progressed since the previous evaluation.
- 17. Patients withGAP often have small amounts of bacterial plaque associated with the affected teeth. Quantitatively, the amount of plaque seems inconsistent with the amount of periodontal destruction. Qualitatively, P. gingivalis, A. actinomycetemcomitans and Bacteroids forsythus frequently are detected in the plaque that is present. Two gingival tissue responses can be found in cases of GAP one is severe, acutely inflamed tissue, often proliferating, ulcerated & fiery red. Bleeding may occur spontaneously or with slight stimulation. Suppuration may be an important feature. This tissue response is considered to occur in the destruction stage, in which attachment & bone are actively lost.
- 18. In other cases,the gingival tissues may appear pink, free of inflammation & occasionally with some degree of stippling, although the last feature may be absent. However, despite the apparently mild clinical appearance, deep pockets can be demonstrated by probing. This tissue response has been considered by Page & Schroeder to coincide with periods of quiescence in which bone level remains stationary. Some patients with GAP may have systemic manifestations such as weight loss, mental depression & general malaise. As seen with LAP, cases of GAP may be arrested spontaneous or after therapy, whereas others may continues to progress inexorably to tooth loss despite intervention with conventional treatment.
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- 21. Radiographic findings : Theradiographic picture in GAP can range from severe bone loss associated with the minimal number of teeth, to advanced bone loss affecting the majority of teeth in the dentition. Prevalence and distribution by age and sex : In the U.S. a national survey of adolescents aged 14 to 17 reported that 0.13% had generalized aggressive periodontitis. Blacks were at much higher risk that whites for all forms of aggressive periodontitis & males were more likely to have GAP than females.
- 22. Risk factors foraggressive periodontitis : o Microbiologic factors o Immunologic factors o Genetic factors o Environmental factors Microbiologic factors : Although several specific microorganisms frequently are detected in patients with LAP, A. actinomycetemcomitans has been implicated as the primary pathogen associated with this disease.
- 23. o A.A producesa number of virulence factors that may contribute to the disease process. o Another study found elevated levels of P.gingivalis, P.intermedia, Fusobacterium nucleatum, C.rectus & Treponema denticola in patients with either localized or generalized aggressive disease. o Electron microscopic studies of localized aggressive periodontitis have revealed bacterial invasion of connective tissue, that reaches the bone surface. o The invading flora has been described as morphologically mixed, but compared mainly of gram negative bacteria including cocci, rods, filaments and spirochetes.
- 24. Immunologic factors : Someimmune defects have been implicated in the pathogenesis of aggressive periodontitis. The human leukocyte antigens (HLA), which regulate immune response, have been evaluated as candidate markers for aggressive periodontitis. Several investigators have shown that patients with aggressive periodontitis display functional defects of PMNs, monocytes or both – which can impair either the chemotactic attraction of PMN to the site of infection or their ability to phagocytic & kill microorganisms.
- 25. Neutrophil migrationto gingival crevice is slower. Mainly in LAP, neutrophils are present with decrease in chemotactic response to variety of chemotactic factors like C5a, FMLP (Formyl peptide), and leukotriene B4. There is also functional decrease in chemotaxin receptors on PMN neutrophil surface….pan receptor defect.
- 26. Neutrophil defectsassociated with Aggressive Periodontitis are Abnormalities in adherence(LAD-1&2) Abnormalities in chemotaxis • pan receptor defect • papillion lefevre syndrome • chediak higashi syndrome Abnormalities in phagocytosis and intercellular killing
- 27. Current studies havealso demonstrated hyperresponisveness of monocytes from LAP patients with respect to their production of PGE2 in response to lipopolysaccharides (LPS) – increased connective tissue or bone loss due to excessive production of these catabolic factors. These PMN and monocyte defects may be induced by bacterial infection or may be genetic in origin. Autoimmunity has been considered to have role in generalized aggressive periodontitis according to Anusaksathien & Dolby, who found host antibodies to collagen, DNA & immunoglobulin G (IgG).
- 28. Genetic factors :LAP is inherited as an autosomal dominant mode Several authors have described a familial pattern of alveolar bone loss and have implicated genetic factors in aggressive periodontitis. Data support the idea that a gene of major effect exists for aggressive periodontitis. Evidence suggests that some immunologic defects associated with aggressive periodontitis may be inherited. Studies also have demonstrated that the antibody response to periodontal pathogen, particularly A.A is under genetic control. As summarized by Tonetti & Mombelli, “it seems that specific genes may be differrent in various populations and / or ethnic groups & therefore true heterogeneity in disease susceptibility may be present. The role of specific genes remains to be elucidated.
- 29. Environmental factors : Theamount & 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.
- 30. Treatment : Localized aggressiveperiodontitis : 1) Extraction 2) Standard periodontal therapy Scaling and root planing Curettage Flap surgery with & without bone grafts Root amputations, Hemisections Occlusal adjustment Strict plaque control * Frequent maintenance visits * Most important 3) Antibiotic therapy : Adjunct to standard therapy Tetracycline (250 mg) four times daily for 14 days every 8 weeks
- 31. Current approach totherapy : Patients having early forms of aggressive periodontitis may respond to standard periodontal therapy. In almost all cases, systemic tetracycline (250 mg of tetracycline hydrochloride 4 times daily for atleast 1 week) should be given in conjunct with mechanical therapy. If surgery indicated, systemic tetracycline should be prescribed with the patient instructed to begin taking the antibiotic approximately 1 hour before surgery. Doxycycline 100 mg / day may also be used. Chlorhexidine rinses should also be prescribed & controlled for several weeks to aid healing & augment plaque control. In refractory LAP cases, tetracycline resistant Actinobacillus species have been suspected. After performing antibiotic susceptibility tests, the clinician may consider a combination of amoxicillin and metranidazole.
- 32. Generalized aggressive periodontitis: In general, the treatment of patients with GAP similar to that of patients with refractory forms of the disease. Monitor the patients more often because of disease progression is faster in younger ind. Monitor & observe patients overall physical status, as weight loss, mental diffusion & malaise have been reported. Currently, monitoring every 3 weeks in less is suggested while the disease is in an active phase.