freeze-dried bone allograft), xenografts (bovine or corral derived) and alloplastic materials (e.g. AgP is a disease that shows significant differences from other periodontal diseases in terms of severity of destruction, rate of progression, response to treatment, etiologic factors and genetic susceptibility criteria. 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]. [17] For instance, diabetes is proved to be associated with periodontitis- it is a major risk factor when glycaemic control is poor.[18]. 1. Kornman and Robertson [104] found modified Widman flap surgery plus tetracycline was effective in areas where the black pigmented bacteroides and A. actinomycetemcomitans load was high. A. actinomycetemcomitans, short (0.4–1 μm), facultative anaerobic, immobile, Gram(−) rod. The patient reported a smoking habit of 15 cigarettes per day. This report defined some characteristic features of the AgP [2, 3]. Gender factor and its role in development of AgP have not become clear. Patients also had increased antibody response against A. Actinomycetemcomitans, Prevotella intermedia (P. intermedia) and Campylobacter rectus (C. rectus) [14]. The prevalence of AgP changes significantly different between geographical regions and between different racial/ethnic origins. Guerrero et al. The diagnosis of aggressive periodontitis can be con­ firmed by different approaches as listed below. Surgical and non-surgical techniques are applied in the treatment of AgP [84]. In long term, active periodontal treatment must followed by maintenance periodontal treatment for preventing attachment and tooth loss. Periodontal treatment is considered in four main phases. Chronic and aggressive periodontitis lesions cannot be distinguished on the basis of histopathologic features (Smith et al., 2010) or microbial colonization profiles (Armitage, 2010), although there is evidence of immunological differ-ences, including the presence of neutrophil abnormalities in … It is essential that all patients undergo a routine periodontal examination to screen for any form of periodontal disease during a dental checkup. Dark red and ulcerated areas are characterized by severe acute inflammatory disease table is detected during the active phase. Learn more. Patients with LAgP between the ages of 21–35 are those who have not been diagnosed and treated before, depending on the severity of the disease and previous treatments, tooth loss, bone defects and gingival recessions are observed [6, 7]. Facebook. Brief introduction to this section that descibes Open Access especially from an IntechOpen perspective, Want to get in touch? Generalized aggressive periodontitis results in rapid destruction of the periodontium and can lead to early tooth loss in the affected individuals if not diagnosed early and treated appropriately. Lee et al. Three studies have reported no association between the carriage rates of the IL1A − 889 (+4845) C → T gene and AgP [65, 66, 67], but one study have found an association with this gene and AgP in Chinese Population [68]. AgP patients who are smoking showed poor clinical respond the periodontal treatment [64]. As the overall treatment concepts and goals for AgP are not significantly different from that of chronic periodontitis, the different treatment phases (cause related therapy; re-examination for response to therapy; definitive therapy; and maintenance) are similar for both types of periodontitis. The authors estimate the prevalence of early-onset periodontitis, or EOP, in U.S. adolescents and describe the clinical features that occur at an early stage in those who have EOP. In the response to dental plaque accumulation, which leads to gingivitis, substantial evidence has been collected to propose large differences between individuals. Regenerative surgical therapy currently available include the use of bone replacement grafts, barrier membranes or guided tissue regeneration (GTR), biologic modifiers like growth and differentiation factors (GDF), and extracellular matrix proteins like enamel matrix proteins (EMD). In some studies platelet size and function found to decrease in GAgP patients due to the consumption of large platelets at sites of periodontal inflammation. This group of diseases includes; neutropenia, hypophosphatasia, leukemias, Cheidak-Higashi syndrome, leukocyte adhesion deficiency, Papillon-Lefevre syndrome, trisomy 21, histiocytosis and agranulocytosis [1]. Surgical treatment may require for the remaining pockets after initial periodontal treatment of AgP. APPOINTMENT REQUEST. Non-surgical and surgical periodontal treatments combined with systemic antibiotics are recommended for the complete eradication of deep periodontal pockets. [15][16], Patients do not have any underlying systemic disease that would contribute to aggressive periodontitis. The virulence factor is serotypically variable and some serotypes are known to be invasive epithelial cells and gingival tissue. Patients are clinically healthy, except for the presence of periodontitis. 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]. [13] A person's genetic predisposition to the condition is determined by a single gene of major effect, inherited as an autosomal dominant trait. 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. Given the prevalence of AgP in Asia; it found 1.8% in Iraq, 0.86% in Israel, 0.47% in Japan and 0.42% in Saudi Arabia [19]. It’s based on principles of collaboration, unobstructed discovery, and, most importantly, scientific progression. Antibiotics: There is evidence that the additional use of systemic antibiotics in conjunction with non-surgical periodontal treatment results in a more favourable clinical response, as compared to just periodontal treatment alone, as it helps to suppress pathogenic bacteria and create a health-associated biofilm. Red complex bacteria named P. gingivalis, T. forsythia and Treponema denticola (T. denticola) were associated with periodontal tissue destruction [31]. [79] and Park et al. Insufficient studies exist that correlate IL-8 polymorphisms with AgP. [50] LAgP has been associated with various abnormalities of host cell function such as; neutrophil abnormalities, reduced chemotaxis, increased superoxide production, reduced receptor expression, reduced phagocytosis and killing of A. Actinomycetemcomitans, impaired leukotriene B4 and signal transduction abnormalities. This is suggested to be protective against wider spread periodontal breakdown. Most studies performed about polymorphisms were limited by sample size and had variations in case inclusion criteria. The localized and generalized forms are not merely different in extent; they differ in etiology and pathogenesis. Shareable Link. It presents immunological alterations, a strong genetic influence, familial aggregation and early onset. Lindhe and Liljenberg [105] treated 16 patients with modified Widman flAgP surgery plus tetracycline (14 days). A healthy periodontium in a Caucasian would appear stippled and pink with a knife edge margin where it abuts the tooth (pigmentation may differ in other races). Only registered users can add explanations . 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. Help us write another book on this subject and reach those readers. The following reasons have been proposed regarding the limited localization of lesions in AgP [8]. level of oral hygiene) and the tissue response to the treatment. The most obvious features of the disease include hasty attachment loss and bone obliteration and genetic aggregation of the teeth. 0 explanations. [3] Estimates of the disease prevalence are 1-5% in the African population and in groups of African descent, 2.6% in African-Americans, 0.5-1.0% in Hispanics in North America, 0.3-2.0% in South America, and 0.2-1.0% in Asia. These is also evidence they produce increased amounts IL-1α and IL-1β which cause osteoclastic bone resorption. Aggressive periodontitis is a low-prevalence, multifactorial disease, of rapid progression and with no systemic compromise. Despite the information generated, roadblocks to a better understanding of “aggressive periodontitis” continue to exist. 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]. [11] The plasma cells produce specific antibodies in response to the periodontal pathogens, which diffuse into the gingival crevicular fluid. There is limited information about polymorphism of FcγR and AgP. First group was received SRP plus 500 mg metronidazole +500 mg amoxicillin three times a day for 1 week, second group was received 200 mg for the first day loading, 100 mg doxycycline for the following 14 days, third group was received 500 mg metronidazole three times a day for 1 week, and the fourth group was evaluated as the control group. High serum antibody levels against A. actinomycetemcomitans were observed in the majority of locally aggressive periodontitis patients. Both systemic and local factors such as smoking and trauma were proposed as risk modifiers that could complicate diagnostic accuracy.2 Overtime this new classification produced an explosion of information. There is a poor serum response against infecting agents, Destruction is present that is not in balance with the amount of local irritants present, Generalized inter-proximal attachment loss on 3 or more permanent teeth, excluding the first molars or incisors. It is also important for a dental practitioner to check for family history of periodontal disease for each patient. 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]. Today, the microbiological profile of AgP has changed from the presence of specific microorganisms to the presence of more complex microbiota [30]. 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. [6], 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. Also Albandar et al. Gingivitis is a non-destructive disease that causes inflammation of the gums. We are IntechOpen, the world's leading publisher of Open Access books. According to the 1999 workshop, the main feature in diagnosing of AgP is that the individual should be medically healthy [1]. ulcerations of the gingiva. Human cytomegalovirus, Epstein–Barr virus type-1 and HSV-1 are also involved in the progression of the disease [41, 42]. Secondary features: The microbial amount is scanty which doesn’t correspond to the severe periodontal breakdown. It usually affects young people, but it can appear at any age, although this is less frequent(3,4). Currently, the available LDA include tetracycline, minocycline, chlorhexidine gluconate and doxycycline, with the mode of delivery being in the form of fibers, chips, polymers and trays. [15] prevalence of AgP in Africa is between 1–5%, in North and mid-Europe Caucasians 0.1%, in South European ~0.5%, in North America ~0.1–0.2% of Caucasians, 0.5–1.0% of Hispanics and 2.6% of Black people, in South America 0.3–2.0%, in Asia 0.2–1.0%. [34][35] The presence of bleeding on probing (BOP) should be noted which is an indicator of active disease. Studies have shown that the total supragingival and subgingival plaque mass is reduced by mechanical treatment. Publishing on IntechOpen allows authors to earn citations and find new collaborators, meaning more people see your work not only from your own field of study, but from other related fields too. Hwang et al. AgP is a multifactorial disease and many etiological factors are required for clinical presentation. Aggressive Periodontitis, Periodontology and Dental Implantology, Jane Manakil, IntechOpen, DOI: 10.5772/intechopen.76878. IL-23 is a pro-inflammatory cytokine and found positively correlated with CP but existing studies how that there is no significant association of IL-23 polymorphisms with AgP [75]. Tonetti and Mombelli (1999) listed the findings of A. actinomycetemcomitans in relation to LAgP [11]. The treatment protocols are based on studies so far. Aggressive periodontitis: A review Vaibhavi Joshipura 1, Umesh Yadalam 1, Bhavya Brahmavar 2 1 Department of Periodontics, Sri Rajiv Gandhi College of Dental Sciences and Hospital, Cholanagar, Bangalore, India 2 Department of Periodontics, Mathikeri Sampige Ramaiah College of Dental Sciences and Hospital, Affiliated to Rajiv Gandhi Health University, Bengaluru, Karnataka, India Antagonistic bacteria against to A. actinomycetemcomitans. [102] concluded that additional applied local (tetracycline fibers) and systemic (500 mg amoxicillin/clavulanic acid) antibiotics showed equally benefits in terms of clinical parameters. The condition is accompanied by bleeding which usually occurs with light stimulation and discharge of the pus. [97] evaluated SRP plus systemic metronidazole and amoxicillin in use on clinical parameters, in total of 41 individuals with GAgP. [28][27], In advanced cases the alveolar bone loss may be depicted as a horizontal bone loss pattern radiographically.[27][28]. To achieve maximum efficacy, drugs must provide some criteria such as; the drug must reach the targeted site of action, remain at an effective concentration and last for an adequate period of time [99]. HLA-9 and HLA-15 antigens have been shown to be associated with AgP [8, 52]. At the end of the study no significant differences were found in term of PD, BOP [93]. In South America, the prevalence of disease was vary among the countries: 0.32–2.6% in Brazil, 0.32% in Chile [19]. [21] In this case, the manifestation of aggressive periodontitis is believed to be the result of genetic mutation, combined with environmental factors.[21]. Host defences involve multiple factors; saliva, epithelium, inflammatory response, immune response and chemical mediators. Periodontal treatment may help to stabilise the disease, but it does not change one's susceptibility to the disease. [4] Males seem to be at higher risk of GAP than females[2]. AgP classified into two categories named localized and generalized aggressive periodontitis. The severity of periodontal tissue destruction is out of proportion to amount of bacteria present . The presence of microorganisms is essential for the initiation of the inflammatory process in periodontal diseases and the factors related to the host are involved in the progress of the disease. Kaner et al. They also concluded P. intermedia was associated with GAgP. Yeasts also were found in samples. If a case of Agp is diagnosed, it is important to screen the patient's family members as well for AgP. It is important to treat and obtain frequent controls of individuals with AgP which is seen in younger patients coexistent rapid attachment and alveolar bone loss. [17] found a high prevalence of AgP as 7.6% in Moroccan children aged 14–19 years. No significant differences found in term of 40 bacteria species in Generalized CP and GAgP [40]. 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