Enamel matrix proteins (amelogenin) which provides new cementum and the formation of new attachment in periodontal defects and growth factors/differentiation factors (platelet-derived growth factor, insulin-like growth factor, fibroblast growth factor, bone morphogenetic protein, transforming growth factor-beta) which play an import role in tissue development and healing are tools for gaining attachment. Kaner et al. Doxycycline is a semisynthetic tetracycline and is effective in the treatment of periodontitis. The main purpose of the treatment is to create a clinical condition that can hold the largest number of teeth in the mouth. The rate of attachment and bone loss is not the same at these times. [34] On probing, patients with AgP should have evidence of significant periodontal pocket depths and loss of attachment (LOA). Secondary features that are often, but not always, present include the following: The amounts of microbial deposits are inconsistent with the severity of periodontal tissue destruction. Tonetti and Mombelli (1999) listed the findings of A. actinomycetemcomitans in relation to LAgP [11]. Aggressive periodontitis commonly occurs in the age group of 15–35 years. These gram-negative microbes are considered the chief aetiological agent of aggressive periodontitis. Four basic factors play role in the pathogenesis of AgP [26]. However, researches are also available that indicates AgP more common in men than women [18, 21]. This is carried out 10–12 weeks following RSD. There is no certain protocol for the use of adjunctive systemic antimicrobials with SRP, but in general suggests that antibiotic intake should start on the day of debridement completion; debridement should be completed within a short time (preferably <1 week) [94]. [13] A person's genetic predisposition to the condition is determined by a single gene of major effect, inherited as an autosomal dominant trait. Tissue destruction in patients with AgP is not directly related to bacterial deposits also personal immune response plays a major role in severity of destruction. [14], 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. specific periodontal microbial pathogens. In South America, the prevalence of disease was vary among the countries: 0.32–2.6% in Brazil, 0.32% in Chile [19]. The motivation and adaptation of the patient is very important in order to control the disease. [12] Patients with localised aggressive periodontitis have large amount of Aggregatibacter actinomycetemcomitans specific IgG2. Aggressive periodontitis (AgP) is a disease characterized by rapid loss of periodontal tissues affecting systemically healthy individuals during adolescence and adulthood, and forms a group of periodontal diseases [1]. LAgP progresses rapidly and bone loss is three to four times greater than CP. Radiographic assessment should be carried out for patients with evidence of periodontitis to observe alveolar bone levels which can help to identify signs of AgP. How? Key words: Aggressive periodontitis, classification, diagnostics, therapy. Due to the recurrence nature of AgP, maintenance is given to for prevention of additional tooth loss and disease recurrence. The researchers noted that the combination of platelet rich plasma and bovine derived xenograft for the treatment of GAgP, provided successful clinical results in large intrabony defects and that prognosis was affected positively even for teeth that were thought to have hopeless prognosis. the distinguishing features of AgP. Localized aggressive periodontitis (LAgP) occurs in 2% of African-American adolescents but only 0.15% of white adolescents. It is known that A. actinomycetemcomitans has virulence factors that can play a role in the development of the disease such as leukotoxin. If this immune response is not capable to control the inflammation process, complex inflammatory cascades are activated. 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. For this reason, the prevalence of the disease in a given population can be determined by the distribution of the population according to the type and proportion of the race and ethnic group. However, because some pathogens can invade into the tissue, or because periodontal instruments are not effective in deep and complex pockets, mechanical treatment is sometimes ineffective [89]. CRP is an acute phase response molecule and increases in an inflammatory condition such as heat, infection, hypoxia and tissue damage. Available from: Localized aggressive periodontitis (LAgP), Generalized aggressive periodontitis (GAgP), Faculty of Dentistry, Department of Periodontology, Pamukkale University, Denizli, Turkey. Prior to starting periodontal treatment, any overhanging or poorly contoured restorations should be modified or replaced. Localized aggressive periodontitis is characterized by circumpubertal onset and attachment loss localized to the first molars and incisors (with involvement of no more than two teeth other than the first molars and incisors). The defects may be a combination of vertical and horizontal defects (Figures 4(a) and 4(b)). Many studies have shown that genetic factors contribute to the pathogenesis of this disease. Following the initial assessment and diagnosis of AgP, a treatment plan is usually developed for each individual undergoing therapy. Common features generally present are: Patients are healthy except for periodontitis Non-surgical and surgical periodontal treatments combined with systemic antibiotics are recommended for the complete eradication of deep periodontal pockets. Some researchers stated that 3–4 controls per year would suffice. Help us write another book on this subject and reach those readers. [39] found the bacteria in diseased sites in Korean AgP patients, descending percentages; Fusobacterium sp., P. gingivalis, Treponema sp., T. forsythensis, P. intermedia and A. actinomycetemcomitans. © 2018 The Author(s). Allografts (e.g. Insufficient antimicrobial agent concentrations may cause the emergence of resistant bacterial strains [88]. Hwang et al. 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 age of onset of the disease can help us diagnose the disease [4]. Personal immune response plays a major role in severity of destruction [44]. It has been stated that Gram(−) microorganisms play a role mostly in microbial dental plaque (MDP). After the treatment performed and provided the health of periodontal tissues, patient should be included in the maintenance program. During this period gingival hyperplasia depending on dental plaque and/or calculus rarely appears [6]. Elevated proportions of periodonto pathogens namely Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis. LAgP patient; (a)-clinical view of the LAgP patient, (b) 7 mm probing depth at distal of the incisor tooth, (c) radiographic view of the LAgP patient. HeadquartersIntechOpen Limited5 Princes Gate Court,London, SW7 2QJ,UNITED KINGDOM. By making research easy to access, and puts the academic needs of the researchers before the business interests of publishers. Among these, orange complex bacteria: P. intermedia, Prevotella nigrescense (P. nigrescense), Parvimonas micra (P. micra), Fusobacterium nucleatum (F. nucleatum), C. rectus, Eubacterium nodatum (E. nodatum) and Campylobacter showae (C. showae) build a bridge between the pathogens seen in the early period of periodontal disease named red complex bacteria. In a metaanalysis authors concluded that photodynamic antimicrobial therapy cannot be suggested as routine with nonsurgical treatment of patients with AgP according to lack of evidence based on the literature [112]. [38] compared subgingival flora in LAgP, GAgP, CP and healthy controls in 69 Turkish people. The combination of 250 mg of metronidazole and 375 mg of amoxicillin, three times a day for 7 days, as an adjunct to SRP, was found to be very effective in suppressing subgingival A. actinomycetemcomitans load [96]. Also, GAgP has been implicated in the pathogenesis of systemic diseases such as uncontrolled diabetes mellitus, AIDS, leukemia, neutropenia, histiocytosis X, syndromes such as Papillon-Lefevre or Cheidak-Higashi, rare inherited diseases such as hypophosphatasia and intraoral symptom of acquired disorders such as granulocytopenia [13]. The inflammatory exudate in the gingival tissues and gingival crevicular fluid is mostly polymorph neutrophils but also includes B cells and plasma cells. Interleukin-1 (IL-1) is a potent pro-inflammatory mediator that is mainly released by monocytes, macrophages and dendritic cells and genetic polymorphisms of IL1 have been studied in association with AgP. There is limited information about polymorphism of FcγR and AgP. The virulence factor is serotypically variable and some serotypes are known to be invasive epithelial cells and gingival tissue. 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