Periodontol 2000 2010: 53: 45-54. In the studies, the methods which have been used to diagnosis of disease such as; whether radiographies is taken or not, differences in diagnostic equipment, different indexing systems etc. Radiographs should be taken separately from each tooth or area affected by the disease once a year. [27], The amount of plaque present is inconsistent with the amount and severity of tissue destruction [26][27] but with a high plaque pathogenicity due to the presence of increased levels of bacteria like Aggregatibacter actinomycetemcomitans (A.a) and Porphyromonas Gingivalis (P.g). 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. Severe attachment and bone loss occur during this period of the disease [10, 11]. Genetic variations may affect the host response to the disease. The rate of attachment and bone loss is not the same at these times. Membranes have been grouped into two major categories: nonresorbable (high-density polytetrafluoroethylene (PTFE) membranes reinforced or not with a titanium framework (e.g. 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. Therefore, it is important for clinicians to treat the disease and maintain periodontal health [83]. 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. A constantly uncontrolled periodontal infection activates neutrophils and make them more effectively stimulated to counteract microbial episodes. Gingivitis is a non-destructive disease that causes inflammation of the gums. After the treatment performed and provided the health of periodontal tissues, patient should be included in the maintenance program. Photodynamic antimicrobial therapy that photosensitizers (toluidine blue, methylene blue, malachite green) are used inside periodontal pockets for increasing the cytotoxic potential of laser light to potential periodontal pathogens. Twelve months after treatment, approximately 1 mm reduction in PD and higher percentage of teeth with attachment gain was observed in test group [98]. [38][39] Early detection of AgP allows intervention to be carried out before extensive periodontal destruction has taken place which further simplifies treatment. *Address all correspondence to: [email protected] Loss of attachment refers to the destruction of periodontium whereas the bone refers to the alveolar bone supporting the teeth. Most studies show comparable disease prevalence in male and female subjects. We are a community of more than 103,000 authors and editors from 3,291 institutions spanning 160 countries, including Nobel Prize winners and some of the world’s most-cited researchers. Many studies have shown that genetic factors contribute to the pathogenesis of this disease. High serum antibody levels against A. actinomycetemcomitans were observed in the majority of locally aggressive periodontitis patients. 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. [21] In this case, the manifestation of aggressive periodontitis is believed to be the result of genetic mutation, combined with environmental factors.[21]. Twenty-five periodontal lesions in seven patients with LAgP divided into three treatment groups: SRP; SRP plus soft tissue curettage; SRP plus modified Widman flap surgery. In this disease bone loss usually wider than CP [8] (Figure 1). After 12 weeks, either of these antimicrobial agents provide significant additional improvement of the clinical parameters [100]. 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]. People with the same clinical characteristics may have different bacterial flora, or people with different clinical characteristics may have the same bacterial flora. The following reasons have been proposed regarding the limited localization of lesions in AgP [8]. Contact our London head office or media team here. The patient is said to have a high genetic susceptibility to aggressive periodontitis. Studies found that smokers have more affected teeth than non-smokers and high levels of attachment loss. The responses of patients with LAgP to initial periodontal care vary in studies. Treatment should be evaluated according to the initial condition. If this immune response is not capable to control the inflammation process, complex inflammatory cascades are activated. [25], LAP begins around the age of puberty where there is interproximal loss of attachment of the first molar, and or incisors[26] on at least two permanent teeth (one which is a first molar) and no involvement of more than two teeth other than the first molars and incisors,[26][27] lack of inflammation and evidence of deep periodontal pocket with advanced bone loss. The disease can progress so quickly that the aggressive nature, radiographs taken at different times, bone loss is easily recognizable [8]. This stage of treatment involves the reassessment of the individual's compliance (i.e. 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]. Also environmental and behavioral factors determine the final clinical outcome. Skip to content. Human leukocyte antigens (HLA) are antigens that regulate the immune response. Periodontal treatment is considered in four main phases. [106], SRP and modified Widman flap surgery plus systemic amoxicillin/metronidazole combination provide periodontal tissue stabilization at a rate 95% over 5 years. By making research easy to access, and puts the academic needs of the researchers before the business interests of publishers. 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. It is highly effective on periodontopathogenic bacteria such as P. gingivalis and P. intermedia which in the “red complex” [95]. The second periodontal treatment phase is surgical periodontal treatment, third phase prosthetic treatment and fourth phase maintenance periodontal treatment. In some studies, P. gingivalis and T. Forsythia have been shown to be an etiological agent for AgP [10, 11]. [2], Therefore, the prevalence of LAP varies considerably between continents, and differences in race or ethnicity seem to be a major contributing factor. The inflammatory exudate in the gingival tissues and gingival crevicular fluid is mostly polymorph neutrophils but also includes B cells and plasma cells. 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]. The impairment of their phagocytic activity results in persistent inflammation in periodontal tissues. Aysan Lektemur Alpan (November 5th 2018). 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. No significant differences found in term of 40 bacteria species in Generalized CP and GAgP [40]. Common features generally present are: Patients are healthy except for periodontitis These controls should be lifelong, but there is no definitive protocol for frequency. Early diagnosis of aggressive periodontitis is important as it can cause rapid permanent destruction of the periodontal tissues. Aggressive periodontitis runs in the patient's family. Anti-infective treatment includes both mechanical and chemotherapeutic approaches and aims to destroy or reduce the microbial dental plaque biofilm which is primary etiological agent of periodontal infections. [102] concluded that additional applied local (tetracycline fibers) and systemic (500 mg amoxicillin/clavulanic acid) antibiotics showed equally benefits in terms of clinical parameters. (2000) have categorised the virulence factors of Aggregatibacter actinomycetemcomitans as follows. GAgP sometimes accompanied by systemic findings such as weight loss, mental depression and fatigue [12]. [20] Usually the loss of attachment is greater than 2mm per year. While bacterial plaque is essential for initiation of disease, it is generally accepted that genetic factors and host immune response play a large role in the disease susceptibility. Elevated proportions of Porphyromonas gingivalis (P. gingivalis) in some populations. 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]. Page et al. [2], Aggressive periodontitis is much less common than chronic periodontitis and generally affects younger patients than does the chronic form. Our team is growing all the time, so we’re always on the lookout for smart people who want to help us reshape the world of scientific publishing. First phase; initial therapy or non-surgical periodontal treatment. Smoking is also a risk factor for AgP [54]. A. actinomycetemcomitans is considered to be the most effective etiologic agent in AgP for about 30 years [28]. In a case series performed by Buchmann et al. 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. immunological features of aggressive periodontitis. In addition, high-degree of antibiotic tolerance has been demonstrated in mature biofilms [94] when tetracycline was unable to suppress A. actinomycetemcomitans, it has been raised a combined use of antibiotics for the treatment of AgP. The most obvious features of the disease include hasty attachment loss and bone obliteration and genetic aggregation of the teeth. Once diagnosed, the sibling of the child or adolescent must also be investigated for the AgP. At the start of the clinical examination of the gingival and periodontal tissues, the dental practitioner would look at the appearance of the gingiva first. It is also important for a dental practitioner to check for family history of periodontal disease for each patient. Four basic factors play role in the pathogenesis of AgP [26]. The GAgP may begin as localized and become more generalized as more teeth are affected over time. According to the workshop in 1999, if the involvement is less than 30%, the disease is localized, if it is not, considered as generalize [1]. Tetracycline is known to have beneficial effects in wound healing regarding its anticollagenase activity [92] . This is due to the suppression of serum IgG2 and antibody against Aggregatibacter actinomycetemcomitans found in smokers. [28][27], In advanced cases the alveolar bone loss may be depicted as a horizontal bone loss pattern radiographically.[27][28]. In the response to dental plaque accumulation, which leads to gingivitis, substantial evidence has been collected to propose large differences between individuals. Aggressive periodontitis is a low-prevalence, multifactorial disease, of rapid progression and with no systemic compromise. [19] The loss can be determined by using a calibrated periodontal probe and taking radiographs of the dentition. Aggressive periodontitis commonly occurs in the age group of 15–35 years. For unknown reasons, A. actinomycetemcomitans may lose its ability to produce leukotoxin. 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. Progression of attachment loss and bone loss may be self-arresting. Dogan et al. varies. These include metronidazole, chlorhexidine, minocycline, doxycycline and tetracycline. The treatment of these patients is quite challenging, due to the absence of a standard treatment protocol for this disease which its etiology is not fully understood, but also because of the rapid progression, severe periodontal tissue loss and recurrence of the disease. IgA is important because of its antiinflammatory function and reduces inflammation by inhibiting IgG and IgM production. [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. 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. [38] compared subgingival flora in LAgP, GAgP, CP and healthy controls in 69 Turkish people. 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. In a recent study performed with patients who affected by GAgP, the authors concluded that existence of a complex cooperative interaction promoted by Herpes Simplex Virus Type-1 (HSV-1) infection, involving Staphylococcus aureus (S. aureus) and the periodontopathogens P. gingivalis, T. forsythia, and Fusobacterium periodonticum (F. periodonticum), that could promote an accelerate progression of lesions of GAgP [37]. In some studies, it has been reported that spirochetes are rarely or not present in LAgP lesions [32, 33], in contrast some authors reported that there is a high number of spirochetes in lesions [34, 35]. HeadquartersIntechOpen Limited5 Princes Gate Court,London, SW7 2QJ,UNITED KINGDOM. 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]. 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 no significant subgingival and supragingival calculus in patients with LAgP. How? The age of onset of the disease can help us diagnose the disease [4]. Want to get in touch rapid permanent destruction of the disease [ 41, 42 ] severe destruction... Studies investigating polymorphism on the gene that encoded il-10 were not significant [ 71, 72 ] ).!, Oana Craciunescu and Otilia Zarnescu AgP [ 10, 11 ] in use on parameters! Of periodontal disease for each individual undergoing therapy issue in AgP [ 26 ] is... Both Porphyromonas gingivalis and Tannerella forsythensis ( T. forsythensis and C. rectus [ 14 ] dominant in saliva characterized! It presents immunological alterations, a treatment plan is usually developed for each.... 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While some are related to disease progression of the bacteria found in smokers the susceptibility for severe aggressive.! Existing dental plaque is also important to develop the periodontal disease that can be divided into two sub-categories these!

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