Dark red and ulcerated areas are characterized by severe acute inflammatory disease table is detected during the active phase. Some researchers suggested monthly checks during the first 6 months after the treatment finished. 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. Many studies have shown that genetic factors contribute to the pathogenesis of this disease. Phagocytes are essential in resolving inflammation. In Europe it has relatively low prevalence been observed; 0.1% in Denmark, 0.1% in Finland, 0.5% in Italy, 0.1–0.3% in Netherlands, 0% in Norway, 0.11–0.13% in Switzerland, 0.02–0.8% in United Kingdom [19]. In a study red complex bacteria found in that of Generalized CP and GAgP. Pathogenic microorganisms, especially P. gingivalis and Tannerella forsythensis (T. forsythensis) are related to disease progression [10, 11]. In studies involving IL-4 which have anti-inflammatory properties, no association was found between AgP and genotype encoding this cytokine [69]. IL-17 plays an important role in natural and acquired immune response; there is a study in mice demonstrating that IL-17 receptor trigger bone loss in infectious conditions [73]. Each graft material showed a decrease in defect and pocket depth although no significant differences between the different grafting materials were found in terms of hard-tissue or soft-tissue changes. 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. Insufficient antimicrobial agent concentrations may cause the emergence of resistant bacterial strains [88]. No significant differences found in term of 40 bacteria species in Generalized CP and GAgP [40]. GAgP; is characterized by diffuse attachment and bone loss affecting at least three permanent teeth other than first molar and incisor teeth, usually seen in young adults, where poor serum antibody responses to infectious agents occur [10]. [79] and Park et al. 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]. These controls should be lifelong, but there is no definitive protocol for frequency. [36] If the distance between the ACJ and alveolar bone crest is more than 2-3mm then there is a possible suggestion of AgP. In this phase, the patient should be informed by the doctor about the role of the patient, the severity of the illness and the risk factors. 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. Removal of plaque retentive factors: Local plaque retentive factors such as mal-positioned teeth, overhanging restorations, crown and bridgework, partial dentures and fixed/removable orthodontic appliances can increase the risk of periodontal disease and prevent successful treatment and resolution of associated pockets. This stage of treatment involves the reassessment of the individual's compliance (i.e. Aggressive periodontitis is a low-prevalence, multifactorial disease, of rapid progression and with no systemic compromise. Red complex bacteria named P. gingivalis, T. forsythia and Treponema denticola (T. denticola) were associated with periodontal tissue destruction [31]. Antagonistic bacteria against to A. actinomycetemcomitans. To understand the pathogenesis of this complex disease multicenter studies and large sample sizes are required. The diagnostic features of the disease are characteristic, but the clinical presentation and patterns of destructions may vary between patients. In GAP, the clinical appearance of the disease resembles chronic periodontitis. Local Aggressive Periodontitis Aggressive periodontitis is a classification of periodontal disease that can be divided into two sub-categories; these two sub-ca. The following reasons have been proposed regarding the limited localization of lesions in AgP [8]. It has also been found that a low T-helper to T-suppressor ratio is found in aggressive periodontitis which may alter local immune regulation. As a result of 5-year follow-up, successful clinical results were obtained and radiological bone fill in angular bony defects. Frequent follow-ups should not be neglected in these patients. Histopathological features of chronic and aggressive periodontitis. [49] It is thus necessary to attend frequent review appointments at the dentist to ensure there is no relapse of the disease, and that the periodontal health is maintained after active periodontal therapy. This is because AgP may have an autosomal dominant inheritance pattern which suggests that up to 50% of siblings could be affected if one parent has the disease. 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. Bacterial content and host defense clearly play an important role in the disease. ONLINE PHYSICIAN REFERRAL. A. actinomycetemcomitans affects the host response in many ways after colonization in first molars and incisors: A actinomycetemcomitans secretes a factor that inhibits Polymorphonuclear leukocytes (PMNL) chemotaxis. [28][29] The periodontal tissue also exhibits minimal signs of inflammation clinically[30] and show a robust response with serum antibodies to pathogens. Lee et al. 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. [57] investigated these two molecules in AgP patients. They are implicated in the development of aggressive periodontitis by triggering inflammatory response in periodontal tissue. Aggressive periodontitis is more common than a lot of people think, nevertheless many people are unaware of the symptoms and occurrence of this disease. [12] Patients with localised aggressive periodontitis have large amount of Aggregatibacter actinomycetemcomitans specific IgG2. HLA-9 and HLA-15 antigens have been shown to be associated with AgP [8, 52]. [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. Aggressive periodontitis The practitioner should be aware that a small proportion of adolescents may suffer from aggressive periodontitis. It is known that A. actinomycetemcomitans has virulence factors that can play a role in the development of the disease such as leukotoxin. The condition is accompanied by bleeding which usually occurs with light stimulation and discharge of the pus. The other response is known as a period of quiescence, where gingival tissue may appear with no inflammation, pink appearance with some possible stippling. PD, marginal recession, relative attachment, probing bone and radiographic bone levels were measured at the beginning and at 12 months reentry. [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%. Smith M, Seymour GJ, Cullinan MP. [65] could not find any accociation.CD14 and Tolllike receptors (TLRs) are extra and intracellular receptors such as recognize pathogen-associated molecules on Gram(+) and Gram(−) bacteria and mediate the production of cytokines required for effective immune response. In some studies, P. gingivalis and T. Forsythia have been shown to be an etiological agent for AgP [10, 11]. Xajigeorgiou et al. In a study smoking found to related disease activity and progression in GAgP but it is not associated with LAgP [62]. In a theory, viral peptide binding and presentation to T cells via HLA-A9 or HLA-B15 is not sufficient for activating immune response properly resulting AgP with severe periodontal destruction [53]. The periodontal therapy carried out at this stage is of a non-surgical approach, which is aimed at the removal of supra- and sub-gingival plaque and calculus deposits, to decrease the microbial load, bacteria biofilm, and calculus from the periodontally involved sites.[44]. The virulence factor is serotypically variable and some serotypes are known to be invasive epithelial cells and gingival tissue. The treatment protocols are based on studies so far. These results may explain the severity of the lesions by delaying the immunological response against to AgP. During this period gingival hyperplasia depending on dental plaque and/or calculus rarely appears [6]. AgP patients who are smoking showed poor clinical respond the periodontal treatment [64]. A Japanese study reported an association for a composite genotype of the Fc cRIIIa N allele and the Fc cRIIIb +141 R allele in AgP [77] in contrast in a stud performed with Caucasian population there is no association found in term of this gene [78]. [28][27], In advanced cases the alveolar bone loss may be depicted as a horizontal bone loss pattern radiographically.[27][28]. Additional metronidazole + amoxicillin or metronidazole plus SRP have been effective comparing the other groups. This is due to the suppression of serum IgG2 and antibody against Aggregatibacter actinomycetemcomitans found in smokers. In clinical trials, the success of treatment is assessed by considering the probing depth (PD), clinical attachment level (CAL) and bleeding on probing (BOP) using conventional periodontal instruments. [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. As well as Aggregatibacter actinomycetemcomitans being associated with this, the synergism of the disease also accounts for both Capnocytophaga spp and Porphyromonas gingivalis.[5]. Comparison of the clinical features of chronic and aggressive periodontitis. The disease is most commonly seen in African-Caribbean (80%) and least Norwegian (0.2%) [20]. 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. 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. GAgP patient; (a) clinical view of the GAgP patient, (b, c) increased probing depth around the teeth, (d) radiographic view of the GAgP patient. Insufficient studies exist that correlate IL-8 polymorphisms with AgP. Studies found that smokers have more affected teeth than non-smokers and high levels of attachment loss. For unknown reasons, A. actinomycetemcomitans may lose its ability to produce leukotoxin. This response is known to be present in the destructive phase, where there is presence of bone and attachment loss. In areas where periodontal tissue destruction occurs in aggressive periodontitis patients, 90% of A. actinomycetemcomitans are found. [102] concluded that additional applied local (tetracycline fibers) and systemic (500 mg amoxicillin/clavulanic acid) antibiotics showed equally benefits in terms of clinical parameters. Twitter. There is a positive association with HLA-A9 and negative relationship with HLA-A2 and HLA-B5 have shown in patients with AgP [54]. Adjunctive use of metronidazole plus amoxicillin, metronidazole alone or clindamycin in patients with GAgP results in well clinical improvements comparing with the use of doxycycline for a similar amount of time or with SRP alone [88]. radiographic evidence of bone loss. 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. Studies of families, twins and sibling pairs have provided strong evidence for a genetic basis for aggressive periodontitis. At the end of the study SRP alone unable to suppress A. actinomycetemcomitans in periodontal lesions, in contrast SRP plus soft tissue curettage and modified Widman flap surgery succeeded [103]. compared local chlorhexidine chip and ministration and systemic amoxicillin plus metronidazole combination in addition to SRP on clinical parameters in GAgP patients. In line with this concept, it has been shown from the initial research attempts on early-onset periodontitis forms that affected individuals, suffer from metabolic imbalance or hereditary host response defects. There are studies demonstrated that the post-treatment attachment level can be maintained despite the risk of recurrence of the disease [85, 86]. T. forsythensis and C. rectus found the lowest frequency in LAgP. Tumor necrosis factor (TNF) is a pro-inflammatory cytokine which has the potential to stimulate the production of secondary mediators, including chemokines or cyclo-oxygenase products, amplifying the degree of inflammation. In the passive period, the clinical image is especially similar to that of healthy individuals in terms of color, shape and consistency. If a case of Agp is diagnosed, it is important to screen the patient's family members as well for AgP. [7] Fives Taylor et al. Only registered users can add explanations . They also concluded P. intermedia was associated with GAgP. 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. 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. This chapter is distributed under the terms of the Creative Commons Attribution 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The genetic factors that may be involved in the pathogenesis of AgP, have been investigated by considering the immune system regulated by genetic factors and that certain genetic polymorphisms may disrupt the defense system against the agent that infects the immune system. [38][39] Early detection of AgP allows intervention to be carried out before extensive periodontal destruction has taken place which further simplifies treatment. When examined by more advanced techniques, the presence of A. Actinomycetemcomitans, Capnocytophaga sputigena (C. sputigena), mycoplasma strains and spirochetes has been defined [8]. Elevated proportions of Porphyromonas gingivalis (P. gingivalis) in some populations. 0 explanations. 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. The motivation and adaptation of the patient is very important in order to control the disease. This page was last edited on 30 December 2020, at 23:28. Human leukocyte antigens (HLA) are antigens that regulate the immune response. It usually affects young people, but it can appear at any age, although this is less frequent(3,4). 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