Galore International Journal of Health Sciences and Research Vol.3; Issue: 2; April-June 2018 Website: www.gijhsr.com Review Article P-ISSN: 2456-9321

Etiology and Pathogenesis of : A Mini Review

Dr. Amit Mani1*, Dr. Rosiline James2*, Dr. Shubhangi Mani3**

1Professor and HOD, 2Post Graduate student, 3Professor, *Dept. of Periodontics, **Dept. of , Pravara Institute of Medical Sciences, Loni, Maharashtra, India.

Corresponding Author: Dr. Rosiline James ______

ABSTRACT  Elevated proportions of periodonto pathogens namely Aggregatibacter Periodontitis is a common gum disease affecting actinomycetemcomitans and many individuals worldwide. It may be . associated with systemic diseases, auto immune disorders, hormonal changes, syndromes or may  Abnormal phagocytic functions. not be associated with no such factors. Plaque is  Elevated production of prostaglandin E2 considered to be a monster to initiate mostly or a (PGE2) and interleukin‐1β (IL‐1β) majority all the diseases affecting the gingival, which are pro inflammatory mediators periodontia or the tooth. It sometimes may not in response to bacterial endotoxins. initiate but may play a significant role in the  The disease is self limiting. progression and severity of the disease. There is a certain balance between the and the The following is the history of the terms immune response from the host individual. The coined by several authors. imbalance causes the prevalence of pathogenic Gotileb (1923) diffuse atrophy of the bacteria to multiply and also the addition of the alveolar bone pro inflammatory mediators to cause periodontal Gotileb (1928) deep cementopathia Wannenmacher (1938) parodontitis marginalis destruction and eventually . progressiva. Aggressive Periodontitis is a unique disease World Workshop in affecting the causing irreparable Periodontics (1966) Chaput (1967) & Butler (1969) juvenile periodontitis damage. Early diagnosis and the specific World Workshop in Early Onset Periodontitis treatment is the key to the success of therapy. ClinicalPeriodontics (1989) World Workshop in Aggressive Periodontitis Periodontics Key words: Periodontitis, periodontia. [2]

INTRODUCTION AND Classification: 1. According to the location: BACKGROUND Periodontitis is an opportunistic  Localized Aggressive Periodontitis disease caused due to the imbalance  Generalized Aggressive between the bacteria and the host response. Periodontitis Why is it so unique? Following are the primary features. Localised aggressive Periodontitis (LAP):  Medical history is non contributory. Localised Aggressive Periodontitis is localized in nature and doesn’t involve all  Rapid attachment loss and bone teeth in the dentition. destruction is seen.

 Familial aggregation of cases. [1] A] Clinical characteristics of LAP:

 It is confined to the incisors and first Secondary features: molars or atleast two permanent teeth  The microbial amount is scanty which one of which is a molar and not more doesn’t correspond to the severe than two teeth other than molars and periodontal breakdown. incisors.

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 Lack of local factors such as plaque and  Bacteria antagonistic to Aa colonise the . Clinically there is lack of teeth inhibiting it from further inflammation. But it presents with deep colonization. periodontal pockets.  Aa loses its leucotoxin producing  Distolabial migration of the maxillary ability. incisors with diastema formation.  defect formation. [4]  Increased mobility of the maxillary and mandibular incisors and first molars. Etiology and Pathogenesis:  Hypersensitivity of denuded root A] Bacteria: surfaces is observed to thermal and As plaque is the main culprit for tactile stimuli. Periodontitis, we shall discuss about the  Deep, dull, radiating pain during bacteria being an etiological factor in mastication probably caused by irritation Aggressive Periodontitis (Ag). of the supporting structures by mobile Gram‐negative organisms comprised teeth and impacted food. approximately two‐thirds of the isolates  Periodontal abscesses formation. from deep periodontal pockets of the  Regional lymph node enlargement. individuals suffering from AG. But these  Rate is 3 to 4 times more and severe organisms averaged only about one‐third of than in . the isolates in control sites with normal  Prevalence: Blacks are more prone to gingiva. suffer from LAP. Among whites, The bacteria of interest were A. females are more prone and among actinomycetemcomitans, blacks, men are prone more to have spp., Eikenella corrodens, saccharolytic LAP. [3] Bacteroides‐like organisms now classified  Incidence: Puberty to 30 years of age. as Prevotella spp., and motile anaerobic rods today labelled Campylobacter rectus. B] Radiographic findings: Gram‐positive isolates such as streptococci,  Vertical bone loss around the first actinomycetes, and peptostreptococci. A. molars and incisors which begins around actinomycetemcomitans, Capnocytophaga puberty in otherwise healthy teenagers is spp., and Prevotella spp. were also seen. to a classical diagnostic sign of Localised be the most prominent members of the Aggressive Periodontitis. subgingival microbiota of Periodontitis lesions in the primary dentition. The  “Arc-shaped loss of alveolar bone microbial patterns observed in periodontal extending from the distal surface of the lesions of the primary dentition were more second premolar to the mesial surface of complex than the ones found in LAP the second molar” which is a mirror patients. image seen on both sides. A. actinomycetemcomitans (Aa) gained  Bone defects are usually wider than more importance because of usually seen in chronic Periodontitis. 1. Aa was seen to be less frequent in

periodontally healthy individuals. [5] Burn out phenomena or why does LAP 2. Aa produced leukotoxin, that was affect only specific areas? capable of translocating across epithelial  As molars and incisors are the first to membranes, and could induce disease in erupt in the oral cavity, Aa colonizes the experimental animals and non‐oral sites. teeth and evades host defense causing [6]

periodontal destruction. The host body 3. Elevated levels of serum antibodies to produces opsonic anti bodies to attack Aa was seen in such individuals. Also against invading bacteria preventing they produce antibodies locally against colonization of other sites. this organism at diseased sites. [7]

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4. The subgingival load of Aa could not be The organisms associated with LAP reduced after treatment. [8] and GAP are P. gingivalis, Tannerella Hence avoidance of exposure to this forsythia, and A. actinomycetemcomitans. P. organism becomes a relevant issue in gingivalis produces collagenases and prevention and the elimination of A. proteases, endotoxin and fatty acids. [11] actinomycetemcomitans may be a valid High local and systemic immune response treatment goal. However it can be also against P Gingivalis has been demonstrated transmitted from one to another like mother in patients with GAP. [12] to child or between spouses. [9] There have been studies showing not B] Bacterial damage to Periodontium: all humans are equally susceptible and/or Periodontal breakdown occurs via that there is variation in virulence and two related mechanisms: (1) the direct pathogenic potential. The virulence of A. action of the microbes or their products on actinomycetemcomitans is variable, and the host tissues (2) due to the inflammatory proving the existence of at least one responses. [13] particularly virulent subpopulation of A. Investigations in humans have actinomycetemcomitans. There are five confirmed that Aa is able to translocate serotypes of Aa namely a, b, c, d, e. Each across the and invade serotype was found to be present in different the connective tissue. [14] Apical spread of populations worldwide. bacteria is controlled by the first line of All Gram‐negative bacteria are defense consisting of mechanisms such as enveloped by two membranes and the outer the high turnover of junctional epithelium is rich in endotoxin. This has a lipid and a keratinocytes, the outward flow of polysaccharide part and is therefore crevicular fluid, and the directed migration frequently termed lipopolysaccharide (LPS). of PMNs through the junctional epithelium; LPS is set free when bacterial cells die or the efficiency is highly enhanced by the multiply. A. actinomycetemcomitans presence of specific antibodies and secretes membrane vesicles that can serve as complement fragments in the gingival transport vehicles to spread endotoxin and crevicular fluid. [15] pathogenic substances produced by the bacteria. LPS activate host cells, C] Host response to bacteria: macrophages thereby secreting Local inflammatory responses are inflammatory mediators such as shown by an intense recruitment of PMNs prostaglandins, IL‐1β, and tumor necrosis both within the tissues and into the factor‐alpha (TNF‐α). Also Aa is periodontal pocket. B cells and immunosuppressive, collagenolytic and antibody‐producing plasma cells represent a inhibits neutrophil chemotaxis. significant component. IgG‐producing The leucotoxin destroys PMNs and cells, with a lower proportion of macrophages. Leucotoxin was seen to be IgA‐producing cells. [16] Local produces highly by serotype b (now known IgG4‐producing cells seem to be elevated. as JP2 clone) which was seen in the African It has been noticed that there is a depressed descent. A. actinomycetemcomitans is T‐helper‐to‐T‐suppressor ratio as compared considered an opportunistic pathogen or to both healthy gingiva and peripheral blood commensal bacterial species as a whole. due to altered local immune regulation. However, at least one distinct [17,18] subpopulation, the JP2 clone, truely displays Local inflammatory responses are the properties of a pathogen in at least one characterized by high levels of PGE2, group of humans of North and West African IL‐1α, and IL‐1β in both gingival crevicular descent. [10] fluid and tissue. [19] PGE2 production is highly elevated in AgP subjects in

Galore International Journal of Health Sciences and Research (www.gijhsr.com) 6 Vol.3; Issue: 2; April-June 2018 Amit Mani et al. Etiology and Pathogenesis of Aggressive Periodontitis: A Mini Review comparison to healthy and chronic CONCLUSIONS Periodontitis patients. Also specific Aggressive Periodontitis both antibodies against AgP‐associated generalized and localised are severe in the microorganisms; [20] have also been detected rate of progression and extent. Early in crevicular fluid from AgP lesions. diagnosis is very essential for the successful Substantial titers of antibodies against A. a treatment and good prognosis. It has been and P. g have been detected in the serum of noted that antibiotic therapy with AgP mechanical can give a positive patients. outcome. It could be prevented in families Anti‐A. actinomycetemcomitans with history of Aggressive Periodontitis serotype polysaccharide IgG2, is considered with periodontal screening, maintaining to be protective against AgP. [21] Patients good , eliminating the risk suffering from GAP, frequently show both factors and the causative micro organisms. low levels of serum antibodies against P. gingivalis and low levels of antibody REFERENCES avidity, indicating a specific inability of 1. Lang, N.P., Bartold, P.M., Cullinam, M. et some GAP patients to cope effectively with al. (1999). International Classification the mentioned bacteria. Importantly, Workshop. Consensus report: Aggressive however, both titers and avidity of periodontitis. Annals of 4, 53. antibodies reacting with P. gingivalis can be 2. Tonetti, M. & Mombelli, A. (1999). Early improved as a result of a successful onset periodontitis. Annals of periodontal therapy. Periodontology 4, 39–53. PMNs of some LAP and GAP 3. Löe, H. & Brown, L.J. (1991). Early onset patients show decreased migration and periodontitis in the United States of antibacterial functions which is a minor America. Journal of Periodontology abnormality, clusters in families like AP. [22] 62,608–616. Other reports indicate that PMN 4. Thoma KH, Golman HM. Wandering and abnormalities in LAP patients may be, the elongation of the teeth and pocket formation result of a hyper inflammatory state in paradontosis. J. Am Dent Assoc 1940; resulting in the presence of 27: 335 5. Löe, H. & Brown, L.J. (1991). Early onset pro‐inflammatory cytokines in the serum of [23] periodontitis in the United States of some AgP patients. America. Journal of Periodontology 62, 608–616. D] Environmental aspects of host 6. Zambon, J.J., Umemoto, T., De Nardin, E. susceptibility: et al. (1988). Actinobacillus Cigarette smoking is a risk factor for actinomycetemcomitans in the pathogenesis patients with generalized forms of AgP. [24] of human . Advances in Smokers with GAP had more teeth affected Dental Research 2, 269–274. and greater attachment loss than patients 7. Listgarten, M.A., Lai, C.H. & Evian, C.I. with GAP who did not smoke. The (1981). Comparative antibody titers to mechanisms indicate that IgG2 serum levels Actinobacillus actinomycetemcomitans in juvenile periodontitis, chronic periodontitis, as well as antibody levels against Aa are and periodontally healthy subjects. Journal significantly depressed in subjects with of Clinical Periodontology 8, 155–164. GAP who smoke. Since it is a protective 8. Haffajee, A.D., Socransky, S.S. & Ebersole, response against A. actinomycetemcomitans; J.L. (1984). Clinical, microbiological and it leads ti the increase in disease extent and immunological features associated with the severity in these individuals. treatment of active periodontosis lesions. Journal of Clinical Periodontology 11, 600– 618.

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