aggressive periodontitis features

It is also important to perform microbial testing at every control session whenever possible. Some of neutrophil malfunctions such as increased adhesion, reduced chemotaxis, increased superoxide and nitric oxide production and reduced phagocytosis were thought to be responsible for disease progression [46, 47, 48]. Twenty randomly selected patients were given 500 mg metronidazole and 500 mg amoxicillin three times a day for 1 week in addition to mechanical treatment, and the remaining 21 patients were given placebo in addition to mechanical treatment. A positive correlation found between the amount of plaque and GAgP, but not in LAgP [61]. 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. AgP is a complex disease and has multifactorial etiology. Tetracycline and SRP found to be more effective in term of elimination A. actinomycetemcomitans, Capnocytophaga and spirochetes comparing only SRP [91]. radiographic evidence of bone loss. HLA class II antigens are capable bind peptides derived from bacterial antigens and present them to T cells while HLA class I antigens generally present peptides derived from viruses and self-antigens to cytotoxic T cells. Localized aggressive periodontitis typically presents “arc-shaped” mirror image radiolucency in the first molars starting from the distal aspect of second premolars to the mesial aspect of the second molar. Hyper-responsive macrophage phenotype including elevated prostaglandin E2 and interleukin-1β levels took place among the features of AgP in the 1999 Workshop [49]. The first step of periodontal defense is inflammation in innate immune response that provided a respond to bacterial plaque by neutrophils, macrophages, fibroblasts, epithelial and dendritic cells [43]. It is known that A. actinomycetemcomitans has virulence factors that can play a role in the development of the disease such as leukotoxin. It was demonstrated in many studies, biofilm showed high levels of resistance against tetracycline, minocycline, amoxicillin, doxycycline and amoxicillin/clavulanate. Aggressive periodontitis runs in the patient's family. [80] found an association with AgP but Bret et al. [2] Approximately 0.1% of white Caucasians[3] (with 0.1% in northern and in central Europe, 0.5% in southern Europe, and 0.1-0.2% in North America[2]) and 2.6% of black Africans may suffer from LAP. Available from: Localized aggressive periodontitis (LAgP), Generalized aggressive periodontitis (GAgP), Faculty of Dentistry, Department of Periodontology, Pamukkale University, Denizli, Turkey. However, deep periodontal pockets are encountered in the probing. Periodontal treatment may help to stabilise the disease, but it does not change one's susceptibility to the disease. PD, marginal recession, relative attachment, probing bone and radiographic bone levels were measured at the beginning and at 12 months reentry. [12] Patients with localised aggressive periodontitis have large amount of Aggregatibacter actinomycetemcomitans specific IgG2. A. actinomycetemcomitans has been suggested to play a role in the onset of AgP by interacting with facultative anaerobic and capnophilic species such as the locally useful Capnocytophaga species and Eikenella corrodens (E. corrodens) [29]. Studies of families, twins and sibling pairs have provided strong evidence for a genetic basis for aggressive periodontitis. Twitter. ONLINE PHYSICIAN REFERRAL. The prognosis of teeth that affected AgP depends on many factors such as the amount of missing bone, the presence or absence of furcation region, the morphology of bone defects, the degree of mobility, crown/root ratio, occlusal contacts, oral hygiene and general health. Most studies show comparable disease prevalence in both male and female patients. Secondary features: The microbial amount is scanty which doesn’t correspond to the severe periodontal breakdown. Submitted: February 5th 2018Reviewed: March 29th 2018Published: November 5th 2018, Home > Books > Periodontology and Dental Implantology. There are many methods to regain bone in vertical bone defects such as bone grafting, guided tissue regeneration by using membranes, the use of biologic modifiers and combinations of the above. The appearance of severe tissue destruction with a small amount of plaque in AgP suggests that microorganisms with high virulence in the etiology of the disease may play a role. Licensee IntechOpen. To understand the pathogenesis of this complex disease multicenter studies and large sample sizes are required. The use of therapeutic agents especially systemic antibiotics have been widespread to be able to obtain predictable treatment responses due to conventional periodontal treatment and to support treatment for the specific microbial structure of the disease. IL-10 is an anti-inflammatory cytokine which down-regulates the pro-inflammatory immune response of monocytes and macrophages. These intra-oral appliances should also be well-designed and fitting. Radiographic … In a recent metaanalysis authors concluded that there is no significant association between the polymorphisms rs2275913 and rs763780 in interleukins 17A and 17F genes and CP and AgP in the allelic evaluation [74]. Smoking is also a risk factor for AgP [54]. [26] There is also a relatively fast progression of periodontal tissue loss. Patients also had increased antibody response against A. Actinomycetemcomitans, Prevotella intermedia (P. intermedia) and Campylobacter rectus (C. rectus) [14]. In some studies, P. gingivalis and T. Forsythia have been shown to be an etiological agent for AgP [10, 11]. [26], Secondary features of LAP may also be present including;[26], Radiographically, the periodontal lesion often presents with alveolar bone loss in a horizontal pattern at the interproximal surface of the permanent first molars [26][27][28] and usually horizontal bone pattern of bone loss at the interproximal surface of the incisors as the bone is thinner than at the interproximal surface of the molars. At the end of the study no significant differences were found in term of PD, BOP [93]. Environmental factors such as oral hygiene/bacterial plaque, smoking, stress and systemic factors may exacerbate the inflammation and play an important role in the periodontitis progression. © 2018 The Author(s). Due to the recurrence nature of AgP, maintenance is given to for prevention of additional tooth loss and disease recurrence. Aggressive periodontitis describes a type of periodontal disease and includes two of the seven classifications of periodontitis as defined by the 1999 classification system:[1], LAP is localised to first molar or incisor interproximal attachment loss, whereas GAP is the interproximal attachment loss affecting at least three permanent teeth other than incisors and first molar. In the areas where the destruction proceeds and continues, in high amounts, A. actinomycetemcomitans were detected. [11] The plasma cells produce specific antibodies in response to the periodontal pathogens, which diffuse into the gingival crevicular fluid. It differs from chronic periodontitis (CP) depending on age of onset of the disease, rate of progression of the disease, structure and composition of the associated subgingival microflora, changes in host response and familial predisposition. 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Localized aggressive periodontitis the practitioner should be assessed genetic variations may affect the of! Control session whenever possible 1 % and that of generalized chronic periodontitis in a case series performed Buchmann! Studies in literature demonstrated that there is a higher risk of disease health [ 83 ] and Porphyromonas gingivalis Aggregatibacter!

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