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Aggressive Periodontitis
Aggressive Periodontitis
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Aggressive periodontitis




Why is there localisation of disease to 1st molars and incisors in LAP?

Often subjects present with attachment loss that does not fit the specific diagnostic criteria (AP or chronic periodontitis).

Schenkein et al. 1995: cigarette smoking was shown to be a risk factor for patients with generalized forms of AgP.

Smokers with GAP had more affected teeth and greater mean levels of attachment loss than patients with GAP who did not smoke.

IgG2 serum levels as well as antibody levels against A.a. are significantly depressed in subjects with GAP who smoked.

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Aggressive periodontitis

  2. 2. Juvenile periodontitis Early-onset periodontitis, Page & Baab 1989 Deep cementopathia Gottlieb,1928 Diffuse atrophy of the alveolar bone Gottlieb, 1923 1999 AAP International Workshop for Classification Aggressive periodontitis Chaput & colleagues, 1967 Butler in 1969. HISTORICAL BACKGROUND
  3. 3. Aggressive periodontitis refers to the multifactorial, severe, & rapidly progressive form of periodontitis, which primarily but not exclusively affects younger patients. - Int’l Workshop Classification Of Periodontal Diseases & Conditions (1999)
  4. 4. Aggressive periodontitis Disease of the periodontium occurring in an otherwise healthy adolescent The only teeth affected are 1. First molars 2. Incisors Generalized form, it may affect most of the dentition. Amount of destruction manifested is not commensurate with the amount of local irritants In 1971, Paul Baer characterized by a rapid loss of alveolar bone about more than one tooth of the permanent dentition. Baer PN. The case for periodontosis as a clinical entity. J Periodontol 1971:42: 516–520.
  5. 5. Baer proposed 7criteria to define the disease:-
  6. 6. Early onset of the disease during the circumpubertal period (between 11 and 13 years of age) 1) Age of the patient per se is not a primary criterion for the diagnosis of aggressive periodontitis
  7. 7.  An arc-shaped loss of alveolar bone, extending from the distal surface of 5 to the mesial surface of the 7.  Occurs bilaterally, depicting “mirror images” of each other A distinctive radiographic pattern depicting vertical alveolar bone loss at the first permanent molars and at one or more incisor teeth. Classical case of aggressive periodontitis Atypical cases of aggressive periodontitis  Show bone loss at only one proximal surface of 6, or that  Only the molars are affected and not the incisors. 2)
  8. 8. 3) A rapid rate of disease progression. Baer estimated that, typically, an affected tooth can lose 75% of the alveolar bone support at one or more root surfaces within 5 years of disease initiation. Atypical cases:- Alveolar bone loss progresses only to a certain point & then may remain quiescent for many years.
  9. 9. The disease affects only the permanent dentition. The primary teeth are not affected and are not prematurely exfoliated because of destructive periodontal disease. 4) The amount of local etiologic factors is not commensurate with the severity of periodontal destruction. 5)
  10. 10. 6) The disease has a familial pattern. 7) Predominance in female subjects. Baer reported that cases of aggressive periodontitis have a female to male ratio of approximately 3:1. Black male teenagers > Black female adolescent > white female teenagers > white male adolescents.
  11. 11. The 1999 International Workshop for the Classification of Periodontal Diseases and Conditions defined the entity of AP as being characterized by “3 primary features”:- Rapid loss of attachment and tooth- supporting bone Presence of familial aggregation Subject is otherwise healthy
  12. 12. Workshop defined several secondary features:- 1. Inconsistency of the low amounts of present etiological factors (i.e., plaque) & the observed pronounced tissue destruction. 2. Strong colonization by Aggregatibacter actinomycetemcomitans and, in some populations, Porphyromonas gingivalis. 3. Immunological abnormalities:- a. Hyperresponsive macrophages b. Abnormalities of neutrophil function 4. Self-limiting disease.
  13. 13. American Academy of Periodontology workshop, 1999 Aggressive periodontitis Localized aggressive periodontitis Generalized aggressive periodontitis
  14. 14. Localized aggressive periodontitis (LAP) In 1989 the World Workshop in Clinical Periodontics, categorized this disease as:- “Localized juvenile periodontitis” (LJP)
  15. 15.  Circumpubertal onset (11 - 13 years of age).  Localized attachment loss at incisors and first molars; interproximal attachment loss on at least 2 permanent teeth (one of which is a first molar) and involving no more than two 0r fewer teeth other than first molars and incisors.  Robust serum antibody response to infecting agents.
  16. 16. •Lack of clinical inflammation •Amount of plaque inconsistent with the amount of periodontal destruction. •Presence of deep periodontal pockets Clinical features
  17. 17. •Elevated levels of A.a and P. gingivalis. •Distolabial migration of maxillary incisors - diastema formation •Increasing mobility of maxillary and mandibular incisors & 1st molars •↑ Sensitivity of denuded root surfaces to thermal and tactile stimuli • Deep, dull, radiating pain during mastication.
  18. 18. • Classic diagnostic sign of localized aggressive periodontitis Vertical “arc shaped” bone loss irt molars and incisors • Rate of bone loss is about 3-4 times faster than in chronic periodontitis. Radiographic features
  19. 19. Why is there localisation of disease to 1st molars and incisors in LAP? Some reasons for Site specific destruction
  20. 20. After initial colonization, A.a. evades the host defense Production of PMN chemotaxis-inhibiting factors, Endotoxin, Collagenases, Leukotoxin Allow the bacteria to colonize the pocket and initiate the destruction of the periodontal tissues. After initial attack Immune defenses stimulated Opsonic antibodies are produced Phagocytosis of invading bacteria and neutralization of leukotoxic activity. (may slow or arrest the disease process) 1)
  21. 21. Bacteria antagonistic to A. a may colonize the periodontal tissues and inhibit it from further colonization of periodontal sites in the mouth. 2) 3)A.a may lose its leukotoxin-producing ability for unknown reasons which arrests or impairs the progression of the disease & may avert the colonization of new periodontal sites.
  22. 22. 4) Defect in cementum formation may be responsible for the localization of the lesion. Root surfaces of teeth extracted from patients with localized aggressive periodontitis have been found to have hypoplastic / aplastic cementum.
  23. 23. lesser humoral response LAP patient GAP patient i.e, LAP and GAP would merely be phenotypic variations of the same underlying disease. This assumption is backed by several reports that show a sequence of LAP and GAP in the same individuals over time.
  24. 24. “Burn-out phenomenon”  Initially it was thought that LAP gradually becomes GAP over time. But some cases of LAP don’t show any increased bone destruction; are known to arrest spontaneously, leading to ceasation of disease activity.  Proposed by Ranney.
  25. 25. Encompasses the diseases that were previously classified as generalized juvenile periodontitis and rapidly progressive periodontitis. Generalized aggressive periodontitis (GAP)
  26. 26. Usually affect <30 years of age, but patients may be older. 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. Poor serum antibody response to infecting agents.
  27. 27. Clinical features of GAP 2 gingival tissue responses: Severe, acutely inflamed tissue that is often proliferating, ulcerated, and fiery red- Destructive stage. # Bleeding # Suppuration # Active loss of attachment & bone Tissues appear pink, free of inflammation, & occasionally with some degree of stippling – Non-destructive stage. # Deep pockets # Bone & attachment levels relatively stable(Period of Quiscence)
  28. 28. Radiographic features Severe bone loss associated with the minimal number of teeth to advanced bone loss affecting the majority of teeth in the dentition.
  29. 29. • Often subjects present with attachment loss that does not fit the specific diagnostic criteria (AP or chronic periodontitis). It includes:  Recessions associated with trauma or tooth position,  Attachment loss associated with impacted third molars, removal of impacted third molars,etc. These patients are a high-risk group for AP or chronic periodontitis. Incidental attachment loss
  31. 31. 1. A.a. 2. Capnocytophaga sp 3. E. corrodens 4. P. intermedia 5. Motile anaerobic rods, such as C. rectus 6. Gram-positive isolates were mostly 1. Streptococci 2. Actinomycetes 3. Peptostreptococci Dominant microorganisms 1. Porphyromonas gingivalis, 2. A.a. 3. Bacteroides forsythus LAP GAP (approx. 90%)
  32. 32. A. a has been implicated as the primary pathogen associated with LAP. As summarized by Tonetti and Mombelli, it is based on the following evidence: 1. A.a is found in high frequency (approx. 90%) in lesions characteristic of LAP. 2. Sites with evidence of disease progression often show elevated levels of A.a 3. Many patients with the clinical manifestations of LAP have significantly elevated serum antibody titers to A.a. 4. Clinical studies show a correlation between reduction in the subgingival load of A.a during treatment and a successful clinical response. 5. A.a. produces a number of virulence factors that may contribute to the disease process.
  34. 34. Human leukocyte antigens (HLAs) have been evaluated as candidate markers for aggressive periodontitis. HLA A9 & B15 antigens are consistently associated with aggressive periodontitis Functional defects of PMNs, monocytes, or both :-  Impair the chemotactic attraction of PMNs to the site of infection or their ability to phagocytose & kill microorganisms.  Hyperresponsiveness of monocytes from LAP patients involving their production of prostaglandin E2 in response to LPS Increased connective tissue or bone loss
  36. 36.  Segregation analyses -- autosomal dominant mode of inheritance (Saxen & Nevanlinna 1984, Beaty et al. 1987, Hart et al. 1992, Marazita et al. 1994).  Antibody response to periodontal pathogens, particularly A.a, is under genetic control, and that the ability to mount high titers of specific, protective antibody (primarily IgG2) against A. a may be race dependent.
  37. 37. RISK FACTORS FOR AGGRESSIVE PERIODONTITIS d) Environmental factors
  38. 38. • Schenkein et al. 1995: cigarette smoking was shown to be a risk factor for patients with generalized forms of AgP. • Smokers with GAP had more affected teeth and greater mean levels of attachment loss than patients with GAP who did not smoke. • IgG2 serum levels as well as antibody levels against A.a. are significantly depressed in subjects with GAP who smoked.
  39. 39. Non-surgical therapy Antimicrobial Therapy; Local Delivery Full-Mouth Disinfection Host Modulation Conventional Periodontal Therapy • Surgical Resective Therapy • Regenerative Therapy MANAGEMENT OF AGGRESSIVE PERIODONTITIS
  40. 40. Non-surgical therapy Its effect on aggressive periodontitis is much less clear. For LAP, the effect of scaling and root planing alone represent the first phase of a staged combination therapy. Slots & Rosling Unsal et al GAP responds well to scaling & root planing in the short term (upto 6 mths). However, after 6 months, relapse and disease progression is reported. Gunsolley et al. Haas et al,2008 Sigusch et al,1998 SRP reduced the total sub-gingival bacterial counts and the proportions of certain gram-negative bacteria, but no periodontal pocket became free of A. actinomycetemcomitans.
  41. 41.  Systemic tetracycline (250 mg of tetracycline hydrochloride 4x/day for at least 1 week) in conjunction with local mechanical therapy.  If surgery is indicated, systemic tetracycline 1000mg stat should be prescribed approximately 1 hour before surgery.  Tetracycline resistant A.a:- Amoxicillin-Metronidazole; Ciprofloxacin- Metronidazole Anti-microbial Therapy
  42. 42. Doxycycline, 100 mg/day, may be used instead of tetracycline. Chlorhexidine rinses should be prescribed and continued for several weeks to enhance plaque control and facilitate healing.
  43. 43.  Genco et al treated LAP patients with:- SRP  Systemic administration of tetracycline (250 mg q.i.d x 14 days every 8 weeks). Bone loss stopped, 1/3rd of defects demonstrated an increase in bone level 18 months  Liljenberg and Lindhe treated LAP patients with Systemic administration of tetracycline (250 mg q.i.d for 2 weeks) Modified Widman flap Periodic recall visits (one visit every month for 6 mths, then one visit every 3 mths). The lesions healed more rapidly and more completely
  44. 44. In practice, antibiotics are often used empirically without microbial testing. Empiric use of antibiotics, such as a combination of amoxicillin & metronidazole, may be more clinically sound and cost-effective than bacterial identification & antibiotic-sensitivity testing. Microbial Testing
  45. 45. Associated Microflora Antibiotic of Choice Gram-positive organisms Amoxicillin–Clavulanate potassium (Augmentin) Gram-negative organisms Clindamycin Non-oral gram-negative, facultative rods Ciprofloxacin Pseudomonads, Staphylococci Black-pigmented bacterial, spirochetes Metronidazole Prevotella intermedia, Porphyromonas gingivalis Tetracycline Aggregatibacter actinomycetemcomitans Metronidazole-amoxicillin Metronidazole-ciprofloxacin Tetracycline P. gingivalis Azithromycin Antibiotic Therapy for Aggressive Periodontitis
  46. 46. Generalized Aggressive Periodontitis: Sigusch et al (2001), Xajigeorgiou et al (2006), Guerrero et al (2007) suggested use of Clindamycin + SRP showed increase in clinical attachment gain and reduction in pocket depth Kaner et al (2007) showed use of metronidazole/ amoxicillin given immediately after SRP will be more effective in resolving deep sites in GAP patients.
  47. 47. Local delivery agents including solutions, gels, fibers, chips  Smaller dosages of topical agents can be delivered inside the pocket,  Avoidance the side effects of systemic antibacterial agents  Increases the exposure of the target microorganisms to higher concentrations, of the medication.
  48. 48. - Another approach to antimicrobial therapy. - The concept, described by Quirynen et al, consists of:-  Full-mouth debridement completed in 2 appointments within a 24-hour period  The tongue is brushed with a chlorhexidine gel (1%) for 1 minute,  Mouth rinsed with a chlorhexidine solution (0.2%) for 2 minutes,  Periodontal pockets irrigated with a chlorhexidine solution (1%) Full-Mouth Disinfection Significant reductions in periodontal pathogens up to 8 months after therapy. P. gingivalis and T. forsythia were reduced to levels below detection.
  49. 49. Host Modulation A novel approach in the treatment of aggressive periodontitis and difficult-to-control forms of periodontal disease. Modulates the host response to disease. Tetracyclines Growth factors Enamel matrix proteins BMPs Bisphosphonates NSAIDS
  50. 50. Access surgery • Modified Widman flap procedure effective in reducing PPD. Christersson et al, 1985 • SRP  Tetracycline administration  MWF surgery Lindhe & Liljenberg, 1984
  51. 51. Surgical Resective Therapy  Effective to reduce or eliminate pocket depth  Difficult to accomplish if adjacent teeth are unaffected, (in cases of LAP)  Careful evaluation of the risks versus the benefits of surgery must be considered on a case-by-case basis.
  52. 52. Regenerative surgery • Bone grafting, o Guided tissue regeneration using membranes,  The use of biologic modifiers &  Combinations of the above Designed for the regeneration of steep vertical defects & have very specific indications :- defect morphology, tooth mobility & furcation involvement.
  53. 53. Bone grafting Yukna & Sepe, reported an average defect fill of 80% with FDBA in 12 patients with LAP at re-entry after 12 months. Evans et al evaluated a 4:1 ratio combination of -tricalcium phosphate/ tetracycline, hydroxyapatite/tetracycline or freeze-dried bone allograft/tetracycline in patients with LAP which showed significant decrease in defect depth & pocket depth were detected for each graft material. Hydroxyapatite/tetracycline  -tricalcium phosphate/ tetracycline.
  54. 54. OTHERS 1. Autogenous bone chips (Oshrains and Kaslick – 1981) 2. Osseous coagulum (Burnette and Steroark - 1969) 3. Frozen autogenous hip marrow (De Marco and Scaletter-1970)
  55. 55. PD reduction & clinical attachment gain significantly greater in the PTFE membrane-treated defects than in osseous surgery -treated defects. Sirirat M, Kasetsuwan J, Jeffcoat MK. Comparison between 2 surgical techniques for the treatment of early-onset periodontitis. J Periodontol 1996:67: 603–607 Guided tissue regeneration Esposito et al(2003) reported that use of emdogain can improve clinical attachment level(1.3mm) and reduction in probing depth(1.0mm) compared to flap debridement alone. Enamel matrix proteins
  56. 56. PHOTODYNAMIC THERAPY Study by Rafael R. de Oliveira et al (2009) concluded that PDT and SRP showed good results in the treatment of aggressive periodontitis.
  57. 57. Ozonized water in treatment of AP Effect of ozonized water on oral microorganisms & dental plaque was studied by Nagayoshi et al., (2002). Useful in reducing the infections caused by oral microorganisms in dental plaque. Ramzy et al assessed the clinical and antimicrobial effect of ozonized water in management of aggressive periodontitis, found that ozone has a potent antibacterial effect explained by the fact that it causes disruption of the envelope integrity through peroxidation of phospholipids.
  58. 58.  The duration between recall visits should be usually short during the period after completion of therapy, generally no longer than 3- month intervals.  Monitoring as frequently as every 3 - 4 weeks may be necessary when the disease is thought to be active.  If signs of disease activity and progression persist despite therapeutic efforts, frequent visits and good patient compliance, microbial testing may be indicated.
  59. 59. CONCLUSION Aggressive periodontitis is the multifactorial, severe, & rapidly progressive form of periodontitis, which primarily but not exclusively affects younger patients where the amount of destruction manifested is not commensurate with the amount of local irritants. Surgery and tetracycline is the best option for treatment as the procedure involves the removal of granulation and connective tissue infected with Aggregatibacter actinomycetemcomitans.
  60. 60. REFERENCES
  61. 61. Carranza, 10th & 12th Edition Albandar, J. M. (2014), Aggressive periodontitis: case definition and diagnostic criteria. Periodontology 2000, 65: 13–26. Könönen, E. and Müller, H.-P. (2014), Microbiology of aggressive periodontitis. Periodontology 2000, 65: 46–78. Kulkarni, C. and Kinane, D. F. (2014), Host response in aggressive periodontitis. Periodontology 2000, 65: 79–91. Teughels, W., Dhondt, R., Dekeyser, C. and Quirynen, M. (2014), Treatment of aggressive periodontitis. Periodontology 2000, 65: 107–133.
  62. 62. THANK YOU

Editor's Notes

  • they portray the
    early-onset development of the disease and its
    occurrence in younger age groups.

    Gottlieb attributed this condition to the inhibition of continuous cementum
    formation, which he considered essential for maintenance of the PDL fibers.
    hypothesized that this was a “disease of eruption” and that
    cementum initiated a foreign body response.
  • Baer believed that the variations in the clinical features of aggressive periodontitis are
    caused by the variability in the phase of disease development and whether the disease is diagnosed at an early phase or an advanced phase.
  • No gross deposits of dental calculus, normal clinical appearance of gingiva with no clinical signs of gingival inflammation.
  • Hart et al, 1991 No sex predilection
  • (i.e., not suffering from any systemic disease or condition that could be responsible for the present periodontitis)

  • that are generally found in aggressive periodontitis cases but that
    are not universally necessary to diagnose the disease entity:
  • 2.9 times

    probably caused by irritation of the supporting structures by mobile teeth and impacted food

    Periodontal abscess & lymphadenopathy
  • Bone defects are usually wider than
    usually seen with chronic periodontitis
  • This would localize A. actinomycetemcomitans infection and tissue destruction
  • This was true not only of root surfaces exposed to periodontal pockets but also of roots still surrounded by their periodontium.
  • Generalized aggressive periodontitis in a 28-year-old Caucasian, female, nonsmoking
    patient. A,Clinical views with minimal amounts of calculus and plaque.
  • B,Radiographically, bone loss of 50% or more was present at all
  • It may include initial clinical presentations of periodontitis.
  • GAP patients are frequently sero negative for A.a. or display low titers and avidity.
  • In some studies, A. a either had no significant association with the presence of aggressive disease & A. a often can be detected in
    periodontally healthy subjects, suggesting that this micro-organism may be part of the normal flora in many individuals
  • :- To identify the specific periodontal pathogens
    responsible for disease and to select an appropriate antibiotic based on
    sensitivity and resistance.
  • For example, in a patient with severe horizontal bone loss, surgical resective therapy may result in increased
    tooth mobility that is difficult to manage, and a nonsurgical
    approach may be indicated.
  • Poor results are expected
    in the treatment of horizontal bone loss, furcation
    defects and increased tooth mobility
  • these
    grafting materials in combination with tetracycline
    can result in additional bonefill and resolution of the
    residual osseous defects in patients with localized
    aggressive periodontitis
  • holding off
    the ingrowth of epithelium and connective tissue,
    cells from the periodontal ligament are allowed to
    grow into the defect, resulting in regeneration of the
    periodontal attachment. There are nonresorbable and
    resorbable membranes.
  • (A) Periodontally diseased site before treatment.
    (B) Mechanical debridement using hand curettes. (C)
    Application of the photosensitizer via syringe at the diseased site that contains residual bacteria. Occasionally,
    excess dye solution is removed using water spray. (D)
    Photosensitization is performed using an intensive light by
    a special tip applied in the pocket. Singlet oxygen and other
    very reactive agents that are toxic to bacteria are produced,
    resulting in photochemical disinfection of the periodontal
    pocket. (E) Improved wound healing in the treated site.
  • ×