Aggressive periodontitis

Aggressive Periodontitis is more common in females in their adolescence. Also called as Juvenile Periodontitis.

1. AGGRESSIVE PERIODONTITIS Binaya Subedi BDS, 4 TH BATCH Chitwan Medical College

2. Introduction I t is a severe and rapidly progressing form of periodontitis . Clinical presentation : age : 18-19 yrs gender : F>M

3. TYPES

4. In LAP , the involved teeth are at least two permanent teeth ,in which one is central incisor and the other is 1 st molar Whereas , in GAP the involved teeth are at least 3 permanent teeth except central incisor and 1 st molar

5. Localized aggressive periodontitis History In 1923 : Gottlieb reported as “Diffuse atrophy of the alveolar bone” In 1928 : Gottlieb termed as “Deep cementopathia ” because of continuous cementum formation In 1938 : Wannemacher termed as “ Paradontitis marginalis progressiva ”

6. In 1966 : World Workshop in Periodontics Eliminated the term Periodontosis from periodontal nomenclature The term Juvenile Periodontitis was introduced by Chaput and colleaugues in 1967 and by Bulter in 1969 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 teeth of the permanent dentition

7. In 1989 : World workshop in clinical periodontics categorized this disease as Localized juvenile periodontitis, a subset of board classification of “early onset periodontitis”

8. Onset = puberty Location is 1 st molar/ incisors with interproximal attachment loss on at least two permanent teeth

9. Reasons for localization are : After initial colonization of 1 st permanent teeth to erupt (1 st molars and incisors) A.a . ( Actinobacillus actinomycetemcomitans ) evades the host defences by different mechanism ,including : Production of PMN chemotaxis inhibiting factors Endotoxin Collagenases Leukotoxin and other factors that allow bacterial colonization and destruction of periodontal tissues

10. After initial attack ,immune defences are stimulated to produce opsonic antibodies to enhance the clearance and phagocytosis of invading bacteria and neutralize leucotoxic activity so, colonization of other sites is prevented Attachment of A.a . to tooth surface is prevented by mucopeptide

11. Bacteria antagonists to A.a colonize the periodontal tissue and inhibit A.a from further colonization in the mouth. This would localize A.a infection and tissue destruction. A.a may lose its leukotoxin producing ability for unknown reasons so destruction of periodontal tissue arrested and colonization of new periodontal sites averted A defect in cementum formation may be responsible for the localization of the lesion

12. Clinical features Age : around puberty Characterized as inter-proximal attachment loss on at least 2 permanent teeth, one of which is 1 st molar and other is incisor Striking feature of LAP - lack of clinical inflammation - absence of deep periodontal pockets

13. The amount of plaque n affected teeth is minimal which seems inconsistent with the amount of periodontal destruction present The plaque that present forms a thin biofilm on teeth rarely mineralizes to form calculus Plaque contains elevated levels of A.a and P.g ( Prophyromonas gingivalis )

14. LAP ,progress rapidly ,Rate of bone loss is about three to four times faster than in chronic periodontitis LAP, may include Distolabial migration of the maxillary incisors with concomitant diastema formation increasing mobility of 1 st molar [also known as pathological migration ] Sensitivity of denuded root surfaces of thermal and tactile stimuli

15. Deep,dull ,radiating pain during mastication probably because of irritation of supporting structure by mobile teeth and impacted teeth Periodontal abscess may form and regional LN enlargement may occur

16. Radiographic findings Classical sign : vertical bone loss around incisors and 1 st molar in puberty Arc shaped bone loss extending from distal of 2 nd premolar to mesial surface of 2 nd molar Bone defects wider than chronic periodontitis Mirror image pattern –bilateral symmetrical pattern of bone loss

17. Discontinuity of lamina dura Widening of periodontal space Angular bone loss is evident on the mesial aspect of 46

18. Generalized aggressive periodontitis Clinical characteristics : Occurs in <30 yrs ,but older patients also maybe affected These patients show poor Ab response to the pathogens present GAP is characterized by generalized interproximal attachment loss affecting at least 3 permanent tooth other than 1 st molar and incisor

19. GAP has small amount of bacterial plaque associated with affected teeth Quantitatively amount of plaque seems inconsistent with amount of PDL destruction Two gingival tissue response can be found here ; i) one is a severe acutely inflammed tissue often proliferating, ulcerated and fiery red, bleeding may occur spontaneously or with slight stimulation -attachment and bone are actively lost, suppurative may be an important feature

20. ii) in other cases, the gingival tissue may appear pink, free of inflammation, and occasionally with some doses of stippling feature may be present . Bone level remains stationary Some patients with GAP may have systemic manifestations such as weight loss, mental depression, and general malaise

21. Radiographic findings 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

22. Risk factors for aggressive periodontitis Microbiologic factors - Actinobacillus actinomyctemcomitans is found in high frequency (appro.90%) in lesions characteristic of LAP -primary pathogen also include Prophyromonas gingivalis , campylobacter, Fusobacterium nucleatum , Treponema denticola

23. 2) Immunological factors -function defects of PMNs monocytes or both -hyper responsiveness of monocytes -strong Ab response to A.a 3) Genetic factors -familial pattern of bone loss is one the risk factor 4) Environmental factors -smoking(amount and duration)

24. Prognosis Prognosis depends upon - disease condition whether localized or generalized -degree of destruction at the time of diagnosis - ability to control future progression

25. LAP in general => fair prognosis If severe => poor prognosis In age of puberty, if diagnosed earlier => excellent prognosis and treated with systemic antibiotic therapy and oral hygiene instructions Young patient with GAP doesnot respond well to conventional periodontal therapy therefore, patient often have fair, poor, or questionable prognosis

26. Treatment

27. Non-surgical therapy Antimicrobial therapy -systemic tetracycline: 250mg 4 times daily at least for 1week combination of oral drugs : -doxycycline 100mg BD for 1 st day followed by OD for 14days - amoxycillin and metronidazole given - augmentin ( amoxycillin + clavulanate )

28. Local drug delivery -placed directly in the site -formulated in form of solutions,gels,fibers,chips

29. Standard periodontal therapy -scaling and root planning -curettage

30. Therapeutic modulation -early detection -educate patient and family members Conventional periodontal therapy -patient education about oral hygiene -scaling and root planning -regular recall and maintenance

31. Full mouth disinfection -for removal of all plaque and calculus -consists of full mouth debridement completed in two appointment within 24hrs period -tongue is brushed with a CHX gel 1% for 1min -mouth is rinsed with a CHX solution (0.2%) for 2min -periodontal pockets a re irrigated with a CHX solution

32. Host modulation -sub antimicrobial dose of doxycycline ( anticollagenase effect) treatment planning and restorative consideration -severely compromised teeth are extracted -transplantation of teeth from one site to another -transplantation of developing 3 rd molar to sockets of previously extracted 1 st molar has to be attempted -dental implants

33. Surgical therapy 1. flap surgery with or without bone grafts, root amputation 2. hemi sections 3. occlusal adjustments 4. strict plaque control 5. extraction -involved teeth usually 1 st molar are extracted

34. Maintenance -periodontal condition must be stable i.e. no clinical sign of disease -it consists of : medical history review c omprehensive periodontal and oral examination t horough root debridement and prophylaxis f requent maintenance resists no longer than 3months interval

35. features LAP GAP Age of onset circumpubertal Mostly under 30 yrs of age Microorga . Predominantly A.a Predominantly P.g Local factors Minimal amount of local factors at the site of destruction Abundant amount of plaque and calculus Familial aggregation Strong association Not very clear Pattern of destruction Localized 1 st molar/incisor involvement with interproximal attachment loss on at least two permanent teeth Generalized interproximal attachment loss affecting at least 3 permanent teeth other than 1 st molar and incisors Serum Ab response Rapid and severe loss of alveolar bone Episodic in nature Radiographic findings Vertical or arc-shaped bone loss around 1 st molar and incisors There is generalized extensive bone loss

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