Chronic versus aggressive periodontitis - A comprehensive review from parity to disparity (original) (raw)
Related papers
2016
The aim of this study was to determine the variations in periodontal parameters and microbiological composition in periodontal pockets at the baseline and 3 and 6 months post treatmentin patients with Generalized Aggressive Periodontitis(GAP) undergoing non surgical periodontal treatment combined with chlorhexidine and systemic antibiotics. Medical and dental history was taken from 10 subjects, average age 30.6±2.7 years, diagnosed with GAP. A non surgical periodontal treatment combined with 0.12% chlorhexidine, 875 mg amoxicillin and 500 mg metronidazole every 12 hours for ten days was conducted. At each visit, the following measurements wererecorded: bacterial plaque (BP), bleeding on probing (BOP), probing depth (PD), clinical attachment level (CAL), hypermobility, and furcation lesions, and a sample of subgingivalplaque was taken from the site of the deepest probing depth of each sextant to identify Porphyromonas gingivalis, Treponemadenticola, Tannerella forsythia, Prevotella i...
Periodontal diseases as bacterial infection
Avances en Periodoncia e Implantología Oral, 2005
The periodontal disease is conformed by a group of illnesses affecting the gums and dental support structures. They are caused by certain bacteria found in the bacterial plaque. These bacteria are essential to the onset of illness; however, there are predisposing factors in both the host and the microorganisms that will have an effect on the pathogenesis of the illness. Periodontopathogenic bacterial microbiota is needed, but by itself, it is not enough to cause the illness, requiring the presence of a susceptible host. These diseases have been classified as gingivitis, when limited to the gums, and periodontitis, when they spread to deeper tissues. Classification of periodontal disease has varied over the years. The one used in this work was approved at the International Workshop for a Classification of Periodontal Diseases and Conditions, held in 1999. This study is an overview of the different periodontal disease syndromes. Later, the systematic use of antibiotic treatment consisting of amoxicillin, amoxicillinclavulanic acid, and metronidazole as first line coadjuvant treatment of these illnesses will be reviewed.
Treatment of aggressive periodontitis
Periodontology 2000, 2014
Aggressive periodontitis comprises a group of rapidly progressing forms of periodontal disease that occur in otherwise clinically healthy individuals. It is accepted that, compared with patients with chronic periodontitis, patients with aggressive periodontitis show a more rapid attachment loss and bone destruction that occurs earlier in life. The patient's age when attachment loss is detected is often the criterion used by clinicians to diagnose aggressive periodontitis and to distinguish aggressive periodontitis from chronic adult periodontitis [reviewed by Albandar in this volume of Periodontology 2000 (3)]. Typically, aggressive periodontitis runs in families (familial aggregation), pointing towards a genetic predisposition. These three features (i.e. rapid attachment loss, bone destruction that occurs early in life and familial aggregation) are considered to be the primary features of this disease. In the Workshop for a Classification of Periodontal Diseases and Conditions, the secondary features of aggressive periodontitis were identified as (i) relatively low amounts of bacterial deposits despite severe periodontal destruction, (ii) presence of hyper-responsive macrophage phenotypes, and (iii) increased portions of Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis (46). Recently an entire volume of Periodontology 2000 was devoted to the differences in clinical (5) and histopathological (93) features, epidemiological patterns (24), microbiological (4) and immunological (29, 81) aspects, and genetic and environmental risk factors (94) between aggressive periodontitis and chronic periodontitis. From these reviews it becomes clear that there are indeed major differences between aggressive periodontitis and chronic periodontitis. Despite these major differences, it is not always easy to differentiate these two disease entities clinically. However, from a research perspective, it is essential that these diseases can be, and are, clearly distinguished in order to gain
What is there in a name?": A literature review on chronic and aggressive periodontitis
Journal of Indian Society of Periodontology, 2011
The objective of this review is to bring the reader up-to-date on the current understanding of chronic and aggressive forms of periodontitis and the implications for diagnosis and treatment of these diseases. The only difference between chronic periodontitis and aggressive periodontitis with regard to tissue destruction appear to be perhaps the magnitude, sequelae, and control of the response. While there may be some differences in the cellular infiltrate between these two diseases, the molecular mediators and pathologic processes are generally the same.
Journal of Periodontology, 1996
Epidemiological studies have revealed that advanced destructive periodontal disease affects as many as 7% to 10% of the adult population.1-5 Periodontitis is initiated and supported by the bacteria in dental plaque.6-9 However, the mechanism behind this induction is less clear. Many systemic and local factors participate in the process.10 Among local factors, a finite number of bacterial species have been associated with periodontal tissue destruction.10-13 Most attention has been focused on Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia.14 Other species such as Bacteroides forsythus, Treponema denticela, Campylobacter rectus, Eikenella corrodens, Fusobacterium nucleatum, Capnocytophaga spp, and Peptostreptococcus micros have also been studied.15 Some patients, though meticulous with their oral hy
The objective of this case report was to characterize the subgingival microbiological profiles of two patients with generalized aggressive periodontitis (GAgP) and to evaluate the clinical outcomes of non-surgical periodontal treatment (NSPT) over a 6-months period. Pooled subgingival samples of two patients who referred to our clinic and diagnosed with GAgP were collected and analyzed for the presence of 300 species/phlotypes using Human Oral Microbe Identification Microarray analysis. NSPT was performed within 3-week period. Clinical parameters were measured at baseline, 3 and 6 months after NSPT. Recall visits were performed every 2 weeks during the first 3 months and every 4 weeks up to 6 months. All samples harboured a total of 61 species and 32 species were common in both patients. First patient had 17 and the other had 12 distinct species. High levels of Filifactor alocis, Porpyromonas gingivalis, Campylobacter concisus and rectus, Fusobacterium nucleatum and Desulfobulbus spp. were detected in both patients while Aggregatibacter actinomycetemcomitans was found in none of them. Six months after NSPT, all clinical parameters were improved in two A. actinomycetemcomitans-negative GAgP patients. In addition to well-recognized periodontal pathogens the presence of high levels of Filifactor alocis and Desulfobulbus spp. seem to be associated with GAgP.
Microbiological profile of untreated subjects with localized aggressive periodontitis
2009
Aim: The microbial profile of localized aggressive periodontitis (LAgP) has not yet been determined. Therefore, the aim of this study was to evaluate the subgingival microbial composition of LAgP. Material and Methods: One hundred and twenty subjects with LAgP (n 5 15), generalized aggressive periodontitis (GAgP, n 5 25), chronic periodontitis (ChP, n 5 30) or periodontal health (PH, n 5 50) underwent clinical and microbiological assessment. Nine subgingival plaque samples were collected from each subject and analysed for their content of 38 bacterial species using checkerboard DNA-DNA hybridization.
Subgingival microbial profiles of generalized aggressive and chronic periodontal diseases
Archives of Oral Biology, 2012
Over the last decades, there has been an enthusiastic discussion on the diagnosis and classification of periodontal diseases. 1-3 During this time, many classification systems based on clinical symptoms have been proposed. However, practitioners find that the clinical diagnosis is not always clear cut, and that clinical signs alone may not distinguish different types of disease. Although the last classification system was based on the Infection/Host Response paradigm, 1 knowledge to diagnose periodontal diseases on an etiologic basis is still limited. 3 Consequently, laboratorial methods with diagnostic potential including microbiological tests, 4 analysis of hostrelated factors 5 and genetic parameters 6 have been developed. Although the microbiota associated with periodontal health and disease has been extensively described, 7-9 identification of microbial profiles that could distinguish different a r c h i v e s o f o r a l b i o l o g y 5 7 (2 0 1 2) 9 7 3-9 8 0