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Aggressive periodontitis

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Aggressive periodontitis describes a type of periodontal disease and includes two of the seven classifications of periodontitis:[1]

  1. Localized aggressive periodontitis (LAP)
  2. Generalized aggressive periodontitis (GAP)

Aggressive periodontitis is much less common than chronic periodontitis and generally affects younger patients than does the chronic form.[2][3]

The localized and generalized forms are not merely different in extent; they differ in etiology and pathogenesis.

Aetiology

Microbiology

Of the microflora characterised in aggressive periodontitis, approximately 65-75% of bacteria are Gram-negative bacilli, with few spirochaetes or motile rods present [4]. Aggressive periodontitis is often characterised by a rapid loss of periodontal attachment associated with highly pathogenic bacteria and an impaired immune response. Various studies have associated Aggregatibacter actinomycetemcomitans, formerly known as Actinobacillus actinomycetemcomitans, with aggressive periodontitis. An early study dating back to 1983 explains its prevalence and documents its role in localised aggressive periodontitis [5].

Virulence factors are the attributes of microorganisms that enable it to colonise a particular niche in its host, overcome the host defences and initiate a disease process [6]. Fives Taylor et al. (2000) have categorised the virulence factors of Aggregatibacter actinomycetemcomitans as follows [6].

Promote colonization and persistence in the oral cavity: Interfere with host defences: Destroy host tissues: Inhibit host repair of tissues:
Adhesins Leukotoxin Cytotoxins Inhibitors of fibroblast proliferation
Invasins Chemotactic inhibitors Collagenase
Bacteriocins Immunosuppressive proteins Bone resorption agents Inhibitors of bone formation
Antibiotic resistance Fc-binding proteins Stimulators of inflammatory mediators

Samaranayake notes the evidence for the specific involvement of Aggregatibacter actinomycetemcomitans includes: an increased incidence of it found in subgingival plaque obtained from lesional sites, high level of its antibody which tends to fall following successful treatment, its possession of a wide range of potentially pathogenic products and its elimination with concordant disease regression, following treatment with successful periodontal therapy and adjunctive tetracycline [4].

Porphyromonas gingivalis is a Gram-negative anaerobe associated with the pathogenicity of periodontal disease [7], and aggressive periodontitis is no exception. Greater numbers of both Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans were found in active, destructive periodontal lesions in comparison to non-active sites [7].

Capnocytophaga spp are implicated as prime periodontal pathogens, especially in localised aggressive periodontitis [4]. Both Capnocytophaga spp and Prevotella intermedia were the most frequently detected microorganisms in a study [8], which also noted that Capnocytophaga spp was the most prominent bacteria in subgingival samples of aggressive periodontitis sufferers [8][9].

An impaired ability of peripheral blood lymphocytes to react to chemotactic stimuli is found in the majority of patients suffering from aggressive periodontitis. As well as Aggregatibacter actinomycetemcomitans being associated with this, the synergism of the disease also accounts for both Capnocytophaga spp and Porphyromonas gingivalis [4].

Pathophysiology

Aggressive periodontitis is a multifactorial disease with many complex interactions including host factors, microbiology and genetics.

Host defences involve multiple factors; saliva, epithelium, inflammatory response, immune response and chemical mediators. The inflammatory exudate in the gingival tissues and gingival crevicular fluid is mostly polymorph neutrophils but also includes B cells and plasma cells. The neutrophils may show an intrinsic functional defect and respond abnormally when challenged by certain pathogens [3]. The plasma cells produce specific antibodies in response to the periodontal pathogens, which diffuse into the gingival crevicular fluid. They produce mainly IgG, with some IgA [3]. It has been suggested that these gingival crevicular fluid antibody levels could be potentially useful in the development of a vaccine [4]. Patients with localised aggressive periodontitis have large amount of Aggregatibacter actinomycetemcomitans specific IgG2. This is suggested to be protective against wider spread periodontal breakdown. However, patients with generalised aggressive periodontitis have decreased ability to mount high titres of IgG to Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans.

It has also been found that a low T-helper to T-suppressor ratio is found in aggressive periodontitis which may alter local immune regulation. Monocytes respond to bacterial and inflammatory stimuli with very high levels of local release inflammatory mediators and induce hyper-inflammatory reaction with activation of tissue degrading matrix-metalloproteinases. These is also evidence they produce increased amounts IL-1α and IL-1β which cause osteoclastic bone resorption. These amounts are greatly reduced following treatment [3].

Studies of families, twins and sibling pairs have provided strong evidence for a genetic basis for aggressive periodontitis [1]. A person’s genetic predisposition to the condition is determined by a single gene of major effect, inherited as an autosomal dominant trait. However, for the disease process to initiate the person must be exposed to the presence of periodontal pathogens and potentially also various environmental factors.

Smoking is a generalised risk factor for generalised forms of aggressive periodontitis. Studies found that smokers have more affected teeth than non-smokers and high levels of attachment loss. This is due to the suppression of serum IgG2 and antibody against Aggregatibacter actinomycetemcomitans found in smokers [2].

Features

According to the 1999 International Workshop for the Classification of Periodontal Diseases, aggressive periodontitis was defined according to 3 primary features, in contrast to chronic periodontitis. These features are common for both localized and generalized form of disease.[10][11]

Primary features

  • Patients are clinically healthy.[10]

Patients do not have any underlying systemic disease that would contribute to aggressive periodontitis.[12] For instance, diabetes is proved to be associated with periodontitis- it is a major risk factor when glycaemic control is poor.[13]

  • The rate of loss of attachment and bone loss is rapid.[10]

Loss of attachment refers to the destruction of periodontium whereas the the bone refers to the alveolar bone supporting the teeth.[14] The loss can be determined by using a calibrated periodontal probe and taking radiographs of the dentition.[15] Usually the loss of attachment is greater than 2mm per year.

  • Aggressive periodontitis runs in the patient’s family.[10]

Familial aggregation of aggressive periodontitis is often discovered by taking a thorough medical history of the patient. The patient is said to have a high genetic susceptibility to aggressive periodontitis. Many studies have shown that genetic factors contribute to the pathogenesis of of this disease.[16] In this case, the manifestation of aggressive periodontitis is believed to be the result of genetic mutation, combined with environmental factors.[16]

Secondary features

Secondary features are characteristics which are frequently seen but not always present in every patient diagnosed with aggressive periodontitis.

  • The amount of bacteria is out of proportion to the severity of periodontal tissue destruction.[10]

The amount of bacteria is often indicated by the level of dental plaque.[17] This feature implies that when aggressive periodontitis is present, loss of attachment and bone loss tend to occur even if the plaque level is low.

  • High levels of Actinobacillus actinomycetemcomitans and, in some populations, Porphyromonas gingivalis.[10]

These gram-negative microbes are considered the chief aetiological agent of aggressive periodontitis. They are implicated in the development of aggressive periodontitis by triggering inflammatory response in periodontal tissue.

  • There are abnormalities associated with phagocytes.[10]

Phagocytes are essential in resolving inflammation. The impairment of the their phagocytic activity results in persistent inflammation in periodontal tissues.[18]

  • Hyper-responsive macrophage phenotype.[10]

Due to the increased responsiveness, the macrophages produce excessive levels of inflammatory mediator and cytokine, such as prostaglandin E2 (PGE2) and interleukin-1β (IL-1B).[19] Their hyperactivity is associated with periodontal tissue destruction and bone loss.[20]

  • Progression of attachment loss and bone loss may be self-arresting.[10]

In some patients, the disease may burnout without any cause-related therapy.[21]

Localized vs. generalized forms of aggressive periodontitis

The 1999 Consensus Report published by the American Academy of Periodontology permitted the subdivision of aggressive periodontal disease into localized and generalized forms based on enough individually specific features, as follows:[22]

  • Localized aggressive periodontitis
  • Generalized aggressive periodontitis
    • usually affects patients under 30 years of age
    • poor serum antibody response to infective agents
    • pronounced episodic nature of periodontal destruction
    • generalized presentation affecting at least 3 permanent teeth other than first molars and incisors.
    • More bony destruction and more rapid than the LAP
    • Bleeding, deep pocketing (BPE 4), Periodontal abscess. No gingival inflammation

Severity of periodontal tissue destruction is subclassified in the same fashion as is chronic periodontitis.

Treatment

Treatment generally involves mechanical therapy (non-surgical or surgical debridement) in conjunction with antibiotics. Several studies suggest that these types of cases respond best to a combination of surgical debridement and antibiotics. Regenerative therapy with bone grafting procedures are often selected in these cases due to the favorable morphology of the bony defects which result from the disease.

Aggregatibacter actinomycetemcomitans (Aa) is one of the most efficient causative pathogens in this disease, Tetracycline seems affecting Aa better (250 mg 3 times daily for 2 weeks). However some suggests the use of Metronidazole 400 mg and Amoxicillin 250 mg 4 times daily for 1 week in severe cases. Root planing and maintaining good oral hygiene is required and Periodontal surgery to gain more access to the roots is needed occasionally.

References

  1. ^ Armitage GC (December 1999). "Development of a classification system for periodontal diseases and conditions". Ann. Periodontol. 4 (1): 1–6. doi:10.1902/annals.1999.4.1.1. PMID 10863370.
  2. ^ Albandar JM, Tinoco EM (2002). "Global epidemiology of periodontal diseases in children and young persons". Periodontol. 2000. 29: 153–76. PMID 12102707.
  3. ^ Papapanou PN (November 1996). "Periodontal diseases: epidemiology". Ann. Periodontol. 1 (1): 1–36. PMID 9118256.
  4. ^ a b c d Whiley, R A (2006-11-25). "Essential microbiology for dentistry (3rd edition)". British Dental Journal. 201 (10): 679–679. doi:10.1038/sj.bdj.4814299.
  5. ^ Zambon, J. J.; Christersson, L. A.; Slots, J. (December 1983). "Actinobacillus actinomycetemcomitans in human periodontal disease. Prevalence in patient groups and distribution of biotypes and serotypes within families". Journal of Periodontology. 54 (12): 707–711. doi:10.1902/jop.1983.54.12.707. ISSN 0022-3492. PMID 6358452.
  6. ^ a b Fives-Taylor, P. M.; Meyer, D. H.; Mintz, K. P.; Brissette, C. (June 1999). "Virulence factors of Actinobacillus actinomycetemcomitans". Periodontology 2000. 20: 136–167. ISSN 0906-6713. PMID 10522226.
  7. ^ a b Thiha, K.; Takeuchi, Y.; Umeda, M.; Huang, Y.; Ohnishi, M.; Ishikawa, I. (June 2007). "Identification of periodontopathic bacteria in gingival tissue of Japanese periodontitis patients". Oral Microbiology and Immunology. 22 (3): 201–207. doi:10.1111/j.1399-302X.2007.00354.x. ISSN 0902-0055. PMID 17488447.
  8. ^ a b Nonnenmacher, C.; Mutters, R.; de Jacoby, L. F. (April 2001). "Microbiological characteristics of subgingival microbiota in adult periodontitis, localized juvenile periodontitis and rapidly progressive periodontitis subjects". Clinical Microbiology and Infection: The Official Publication of the European Society of Clinical Microbiology and Infectious Diseases. 7 (4): 213–217. ISSN 1198-743X. PMID 11422244.
  9. ^ Genco, R. J.; Zambon, J. J.; Christersson, L. A. (November 1986). "Use and interpretation of microbiological assays in periodontal diseases". Oral Microbiology and Immunology. 1 (1): 73–81. ISSN 0902-0055. PMID 3295682.
  10. ^ a b c d e f g h i Armitage, Gary C. (2004). "Periodontal diagnoses and classification of periodontal diseases". Periodontology 2000. 34: 9–21. ISSN 0906-6713. PMID 14717852.
  11. ^ Lang, Niklaus; Bartold, P. Mark; Cullinan, Mary; Jeffcoat, Marjorie; Mombelli, Andrea; Murakami, Shinya; Page, Roy; Papapanou, Panos; Tonetti, Maurizio (1999-12-01). "Consensus Report: Aggressive Periodontitis". Annals of Periodontology. 4 (1): 53–53. doi:10.1902/annals.1999.4.1.53. ISSN 1553-0841.
  12. ^ "Managing Aggressive Periodontitis - Decisions in Dentistry". Decisions in Dentistry. Retrieved 2017-12-07.
  13. ^ Preshaw, P. M.; Alba, A. L.; Herrera, D.; Jepsen, S.; Konstantinidis, A.; Makrilakis, K.; Taylor, R. "Periodontitis and diabetes: a two-way relationship". Diabetologia. 55 (1): 21–31. doi:10.1007/s00125-011-2342-y. ISSN 0012-186X. PMC 3228943. PMID 22057194.{{cite journal}}: CS1 maint: PMC format (link)
  14. ^ "Periodontitis, aggressive - Oxford Reference". doi:10.1093/oi/authority.20110803100317810. Retrieved 2017-12-07.
  15. ^ Armitage, Gary C. (2004). "The complete periodontal examination". Periodontology 2000. 34: 22–33. ISSN 0906-6713. PMID 14717853.
  16. ^ a b Vieira, Alexandre R.; Albandar, Jasim M. (June 2014). "Role of genetic factors in the pathogenesis of aggressive periodontitis". Periodontology 2000. 65 (1): 92–106. doi:10.1111/prd.12021. ISSN 1600-0757. PMID 24738588.
  17. ^ Schaeken, M. J.; Creugers, T. J.; Van der Hoeven, J. S. (September 1987). "Relationship between dental plaque indices and bacteria in dental plaque and those in saliva". Journal of Dental Research. 66 (9): 1499–1502. doi:10.1177/00220345870660091701. ISSN 0022-0345. PMID 3476622.
  18. ^ Fredman, Gabrielle; Oh, Sungwhan F.; Ayilavarapu, Srinivas; Hasturk, Hatice; Serhan, Charles N.; Van Dyke, Thomas E. (2011). "Impaired phagocytosis in localized aggressive periodontitis: rescue by Resolvin E1". PloS One. 6 (9): e24422. doi:10.1371/journal.pone.0024422. ISSN 1932-6203. PMC 3173372. PMID 21935407.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  19. ^ Armitage, Gary C. (2004). "Periodontal diagnoses and classification of periodontal diseases". Periodontology 2000. 34: 9–21. ISSN 0906-6713. PMID 14717852.
  20. ^ Shaddox, L.; Wiedey, J.; Bimstein, E.; Magnuson, I.; Clare-Salzler, M.; Aukhil, I.; Wallet, S.M. "Hyper-responsive Phenotype in Localized Aggressive Periodontitis". Journal of Dental Research. 89 (2): 143–148. doi:10.1177/0022034509353397. ISSN 0022-0345. PMC 3096871. PMID 20042739.{{cite journal}}: CS1 maint: PMC format (link)
  21. ^ Asano, Masahiro; Asahara, Yoji; Kirino, Akinori; Ohishi, Mika; Akimaru, Noriko; Hama, Hideki; Sury, Yono; Shionoya, Akemi; Kido, Jun-ichi (2003-09-28). "Case Report of an Early-onset Periodontitis Patient Showing Self-Arrest of Alveolar Bone Loss after Puberty". Nihon Shishubyo Gakkai Kaishi (Journal of the Japanese Society of Periodontology) (in Japanese). 45 (3): 279–288. doi:10.2329/perio.45.279. ISSN 0385-0110.
  22. ^ American Academy of Periodontology (1999). "Consensus report: Aggressive Periodontitis". Ann. Periodontol. 4 (1): 53. doi:10.1902/annals.1999.4.1.53.
  23. ^ AAP In-Service Exam, 2008-B40
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