Herpesvirus‐bacteria synergistic interactions, are likely to comprise an important pathogenic determinant of aggressive periodontitis. Mobility of the affected teeth will be seen towards the later stages of the infection. Background: Recent findings have begun to provide a basis for a causal link between herpesviruses and aggressive periodontitis. The most common form of gingivitis, and the most common form of periodontal disease overall, is in response to bacterial biofilms (also called plaque) that is attached to tooth surfaces, termed plaque-induced gingivitis.Most forms of gingivitis are plaque-induced. Though it can be found in less than two percent of the general population, it's often found in younger patients, even children, and the disease usually affects the first molars more than other teeth. B. Zhang et al., “Tobacco and smoking: environmental factors modify the host response (immune system) and have an impact on periodontal health,”, H. A. Schenkein, J. C. Gunsolley, T. E. Koertge, J. G. Schenkein, and J. G. Tew, “Smoking and its effects on early-onset periodontitis,”, D. A. Apatzidou and D. F. Kinane, “Quadrant root planing versus same-day full-mouth root planing. Grade II furcation involvement was present with molars and maxillary first premolars. The disease is generally found to have a racial and sex predilection, with blacks and male teenagers having higher risk for the disease compared to whites and females, although reports vary between different ethnic groups and populations, with some populations showing prevalence as high as 28.8% [4, 5]. Over the past 20 years, locally delivered, anti-infective pharmacological agents, most recently employing sustained-release vehicles, have been introduced to achieve this goal [60]. The bacteria responsible for periodontitis can enter your bloodstream through gum tissue, possibly affecting other parts of your body. 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. The American Academy of periodontology revised the classification of periodontal diseases in 1999. The majority of the patients refer to dental consultation at this stage of the disease (Figures 3(a)–3(c)). The position of the gingival margin was apical to the CEJ in the labial aspect of 22. Both of these bacterial species produce a number of virulence factors and have the ability to invade host tissues, which protects from mechanical NSPT. The diagnostic features of the disease are characteristic, but the clinical presentation and patterns of destructions may vary between patients. This case report demonstrates the placement of implants in a patient with AgP with successful 18 months follow-up. Poor oral hygiene and smoking may play a role. After adequately anesthetizing the surgical site with infiltration anesthesia and nerve blocks, the first incision (internal bevel incision) 0.5 mm from the gingival margin directing to the crest of the alveolar bone was made. Research has shown that GTR in conjunction with bone grafting has better potential for regeneration compared with either technique alone [74, 84, 85], and this outcome has been confirmed in aggressive periodontitis also with the use of bioresorbable membranes (Bio-Gide) [75, 80]. 2012, Article ID 535321, 17 pages, 2012. https://doi.org/10.1155/2012/535321, 1Department of Periodontics, People’s Dental Academy, Bhopal 462010, India, 2Department of Periodontics, Azeezia Dental College, Kollam 691537, India. In generalized aggressive periodontitis, radiographs may show generalized bone destruction ranging from mild crestal bone resorption to severe extensive alveolar bone destruction depending on the severity of the disease. The patient was put on regular recall appointments for evaluation of the gingival and periodontal status and maintenance therapy. In order to maintain the optimal results got by surgery and to prevent the recurrence of the disease, a lifelong maintenance therapy is mandatory because of the strong genetic susceptibility of the individual to the disease. Copyright © 2012 T. Roshna and K. Nandakumar. Definition  “Aggressive periodontitis” defined as a group of rare, severe, rapidly progressing forms of periodontitis characterized by an early age of clinical manifestation and a distinctive tendency for cases to aggregate in families -Jan Lindhe. The amount of microbial deposits will be inconsistent with the amount of destruction when compared to chronic periodontitis and plaque will be minimal. The severity of the disease appears to be an exuberant reaction to a minimum amount of plaque accumulation and may result in early tooth loss. Danielle Clark, RDH, BSc1/Maria Febbraio, PhD2*/Liran Levin, DMD3* Aggressive periodontal disease is an oral health mystery. The study bacteria occurred in 78-83% (P. gingivalis, T. forsythia, C. rectus) and in 44% (P. intermedia, A. actinomycetemcomitans) of the periodontitis samples, and in 0-19% of the samples from healthy periodontal sites. A recall visit after 2 weeks showed reduction in inflammation and percentage of sites showing bleeding on probing. Use of biologic mediators like growth factors (insulin-like growth factor (ILGF), platelet-derived growth factor (PDGF)) use of platelet-rich plasma which contains PDGF, extracellular matrix proteins like emdogain, etc. Non-surgical therapy It’s effect on aggressive periodontitis is less clear. Additionally use of fluoride mouthwashes is advised to help in remineralization of the exposed root surfaces, and for patients complaining of hypersensitivity, use of desensitizing toothpastes and mouthwashes is mandatory. This leads to two types of presentation at the time of examination. Allogeneic freeze-dried bone (FDBA) mixed with tetracycline powder along with systemic tetracycline has demonstrated a better clinical outcome in treatment of juvenile periodontitis [72]. The patient noticed the spacing about 1 year before, after which she noticed it to be gradually increasing and associated with intermittent episodes of pus discharge which subsided on taking antibiotics as per advice at a local hospital. However, Generalized Aggressive Periodontitis (GAP) manifests when one’s genetic make-up is in concurrence with certain environmental factors and the exposure to pathogenic bacteria causing GAP occurs. A paradigm shift several decades ago elucidated that aggressive periodontitis (AgP) was not a degenerative disorder but a rapid progressive form of plaque-induced inflammatory periodontal disease. Furthermore since it has a tendency for familial aggregation, it is important to do a periodontal examination of siblings and other close blood relatives of the patient which helps in early diagnosis of the disease in the family members. The defects may be a combination of vertical and horizontal defects (Figures 4(a) and 4(b)). Aggressive periodontitis in young people, once known as juvenile periodontitis, affects less than 1% of the population. A postoperative radiograph 6 months later showed a significant bone fill in the molar regions where grafting was done with an increase in bone density of the alveolar crest with corticated bone formations in the crest at the other areas (Figure 8(g)). Curettage for granulation tissue removal was done following which a through subgingival debridement and root planning was performed. Our current understanding of this disease is that specific bacteria invade the oral cavity and the host reacts with an inflammatory response leading to mass destruction of the alveolar bone. Periodontitis generally causes inflammation of the gums, loss of bone in the jaw, and accumulation of tartar deposits both above and below the gum line. It essentially consists of open flap debridement either alone or as a combination with resective or regenerative procedures. Care was taken to fill the graft to a realistic level and not to overpack the defect. Actinobacillus actinomycetemcomitans (Aa) is the bacterium most commonly associated with this disease. gingivalis, and T. denticola were the predominant periodontopathic bacteria of aggressive periodontitis patients, Although A. actinomycetemcomitans was also detected in AgP patients, the prevalence of this bacterium was much lower than lower than that of P. gingivalis. However, mechanistic investigations into the molecular and cellular interaction between periodontal herpesviruses and bacteria are still scarce. Part II,”, M. G. Jorgensen and J. Diode laser treatment has shown a superior clinical and microbiological effect when used along with SRP, compared to SRP alone or laser therapy alone in aggressive periodontitis patients [44]. Some patients may show systemic manifestations such as weight loss, mental depression and general malaise [16]. Including observations on acetone-fixed intra and extracellular proteins,”, T. W. Mabry, R. A. Yukna, and W. W. Sepe, “Freeze-dried bone allografts combined with tetracycline in the treatment of juvenile periodontitis,”, J. T. Mellonig, “Human histologic evaluation of a bovine-derived bone xenograft in the treatment of periodontal osseous defects,”, M. Camelo, M. L. Nevins, R. K. Schenk et al., “Clinical, radiographic, and histologic evaluation of human periodontal defects treated with bio-oss and bio-gide,”, B. Owczarek, M. Kiernicka, E. Gałkowska, and J. Wysokińska-Miszczuk, “The application of Bio-Oss and Bio-Gide as implant materials in the complex treatment of aggressive periodontitis,”, M. L. Nevins, M. Camelo, S. E. Lynch, R. K. Schenk, and M. Nevins, “Evaluation of periodontal regeneration following grafting intrabony defects with Bio-Oss Collagen: a human histologic report,”, R. A. Yukna, J. T. Krauser, D. P. Callan, G. H. Evans, R. Cruz, and M. Martin, “Multi-center clinical comparison of combination anorganic bovine-derived hydroxyapatite matrix (ABM)/cell binding peptide (P-15) and ABM in human periodontal osseous defects. Various commercially available regenerative materials including bone replacement grafts, GTR membranes, enamel matrix derivatives, are in the market for use in periodontal therapy with varying results, and the choice of the material depends on the dentist’s preference and experience with the products helping in clinical judgment of the therapeutic results of individual products and procedures and their cost-benefit ratio. Even children have been known to develop this disease, though the typical patient is an adult younger than 35 at the time symptoms appear. Experts don't yet understand what causes aggressive periodontitis, but they believe it may be linked to the bacterium Aggregatibacter actinomycetemcomitans (Aa). A systematic review,”, F. F. Duarte, R. F. Lotufo, and C. M. Pannuti, “Local delivery of chlorhexidine gluconate in patients with aggressive periodontitis,”, D. Kaner, J. P. Bernimoulin, W. Hopfenmüller, B. M. Kleber, and A. Friedmann, “Controlled-delivery chlorhexidine chip versus amoxicillin/metronidazole as adjunctive antimicrobial therapy for generalized aggressive periodontitis: a randomized controlled clinical trial,”, D. Sakellari, I. Vouros, and A. Konstantinidis, “The use of tetracycline fibres in the treatment of generalised aggressive periodontitis: clinical and microbiological findings,”, P. Purucker, H. Mertes, J. M. Goodson, and J. P. Bernimoulin, “Local versus systemic adjunctive antibiotic therapy in 28 patients with generalized aggressive periodontitis,”, A. Saito, Y. Hosaka, T. Nakagawa, K. Seida, S. Yamada, and K. Okuda, “Locally delivered minocycline and guided tissue regeneration to treat post-juvenile periodontitis. A short communication,”, N. Lang, P. M. Bartold, M. Cullinan et al., “Consensus report: aggressive periodontitis,”, B. Schacher, F. Baron, M. Roßberg, M. Wohlfeil, R. Arndt, and P. Eickholz, “Aggregatibacter actinomycetemcomitans as indicator for aggressive periodontitis by two analysing strategies,”, G. C. Armitage, “Comparison of the microbiological features of chronic and aggressive periodontitis,”, J. M. Goodson, A. C. Tanner, A. D. Haffajee, G. C. Sornberger, and S. S. Socransky, “Patterns of progression and regression of advanced destructive periodontal disease,”, R. C. Page, L. C. Altman, J. L. Ebersole et al., “Rapidly progressive periodontitis. Concentrations at the time of examination and percentage of sites showing bleeding on probing and. The drugs at high concentrations at the time of diagnosis and the specific treatment is ideal! The rapid rate of bone destruction and eventually tooth loss in the etiopathogenesis of the.. Antimicrobial therapy in aggressive periodontitis at a younger age and quiescence [ 15 ] sites... 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