INTRODUCTION: Chronic periodontitis is defi ned as an infl ammatory disease of the supporting tissues of teeth caused by microorganisms in the dental biofi lm, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation and gingival recession. Treatment of chronic periodontitis aims at arresting the infl ammation and stopping the loss of attachment by removal and control of the supra-and subgingival biofi lm and establishing a local environment and microfl ora compatible with periodontal health. The AIM of this study was to evaluate the effectiveness of non-surgical therapy (scaling and root planning) in the treatment of moderate chronic periodontitis. MATERIALS AND METHODS: The study included 30 patients aged between 33 and 75 years, of which 46.7% women and 53.3% men, diagnosed with moderate and, at some sites, severe periodontitis. They were treated with non-surgical periodontal therapy methods (scaling and root planning and curettage if indicated). Additionally, chemical plaque control with rinse water containing chlorhexidine was applied. The diagnostic and reassessment procedures included measuring the periodontal indices of 601 periodontal units before and after the therapy. The indices measured were the papillary bleeding index (PBI), the hygiene index (HI), the probing pocket depth (PPD) and the clinical attachment level (CAL). RESULTS: Signifi cant reduction of plaque and gingival infl ammation was found in all treated patients; we also found a statistically signifi cant reduction of periodontal pockets with clinically measured depth < 5 mm (PD < 5 mm). Pockets with PD > 5 mm did not show statistically signifi cant lower incidence rates probably due to the initially small percentage of deep pockets in the patients studied. There was a statistically signifi cant reduction of all sites with attachment loss, the highest signifi cance found at sites where the attachment loss was greater than 5 mm. CONCLUSION: The results of the study suggest that nonsurgical periodontal therapy is effective in managing the moderate chronic periodontitis. Given a good patient compliance, the antimicrobial periodontal therapy can be quite effi cient in arresting the infl ammatory process and reducing the depth of periodontal pockets; it can also achieve a stable attachment loss level and obviate the need to use a surgical periodontal treatment modality. РЕЗЮМЕ ВВЕДЕНИЕ:Хронический пародонтит представляет собой воспалительное заболевание зубоудерживающих тканей, вызванное микроорганизмами в дентальном биофильме. Заболевание характеризуется прогрессивной деструкцией периодонтального лигамента и альвеолярной кости, формированием карманов и рецессией гингивы. Лечение хронических пародонтитов ставит себе целью элиминировать воспалительный процесс, прекратить потерю периодонтальной связки /attachment/ посредством устранения и контроля супра-и субгингивального биофильма, а также и стабилизировать локальную среду и микрофлору до степени совместимости с пародонтальным здоровьем. ЦЕЛЬ: Работ...
Multifactorial nature of chronic periodontitis is well known. The data indicate that the bacteria of subgingival biofilm (with their presence at high levels, too), as well as the immune response of the organism, genetic components and environmental factors play a significant role in the development of periodontal destructive disease. On the one hand the strong relationship between microorganisms from the “red complex” has been proved. On the other hand the initiation and progression of chronic periodontitis has been verified, as well. The presence of bacterial metabolic products and other substances (lipopolysaccharides, enzymes and toxins) results in increased expression of proinflammatory cytokines and release of active agents leading to the development of a local tissue lesion. Thus, the negative (destructive) side of the immune response is expressed and associated with the immunopathological nature of periodontitis. Literary data testify the importance of interleukin-8 (IL-8) in regulating the inflammatory response to bacterial infection and suggest its association with susceptibility to periodontitis.
Background: Periodontitis is a chronic inflammatory disruption of the periodontal supportive tissues. There are the numerous evidences for his bacterial etiology. Though the occurrence of periodontal bacteria is considered to be the main cause of periodontitis, certain characteristics of the individual immune response may also have inûuence on the disease development and progression, and on the treatment outcomes. There are some reports that attempt to identify genetic factors associated with periodontitis including polymorphisms of interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) genes. We were interested from the distribution of several genotypes of the cytokines: interleukin-6 -(G-174C) and (G-597A), lymphotoxin-α (A+252G), and tumour necrosis factor-alpha (G-308A) in patients with chronic periodontitis.Aim: To investigate the association of chronic periodontitis with certain gene polymorphisms of interleukin-6 (IL-6), Lymphotoxin-α, and tumor necrosis factor-alpha (TNF-α).Material and methods: The study included 30 patients with moderate or severe chronic periodontitis, and 10 persons with healthy periodontium. Total genomic DNA was extracted from the buccal epithelial cells. TNF-A (G-308A), IL-6 (G-174C), IL-6 (G-597A) and LT-A (A+252G) genes polymorphisms were analyzed by Polymerase chain reaction (PCR).Results: Outcomes showed a large variety in genotype's distribution in the investigated groups. No important difference was observed in the distribution of IL-6, TNF-α and LT-α genotypes between chronic periodontitis patients and controls in this study be reason of the small studied group. However, a signiûcant difference in the LT-α was observed -a prevalence of the genotype GG in patients with severe periodontitis. In relation with IL-6 (G-597A) and IL-6 (G-174C) genotyping -in both of them in patients with severe periodontitis was occurred most frequently the genotype GG. In patients with periodontitis the frequency of genotype GG of TNF-α (G-308A) was significantly increased. Conclusion:The assessment IL-6 (G-597A) and IL-6 (G-174C), and TNF-α (G-308A) revealed that genotype GG was moderate associated with chronic periodontitis in Bulgarian individuals. As a result of these findings we may suppose that the G allele may play an important role in the de-velopment and progression of periodontal disease in this population. The frequency of LT-A (A252G) was significantly greater in severe periodontitis patients in this study.
Today, it is known that pathogenic bacteria are the key factors for the initiation of periodontal disease, but the host response and the severity of clinical expression are largely determined by genetic susceptibility and environmental factors. There is evidence that the individual response to the environment and variations in the immune response in periodontitis are associated with genetic factors. Of particular interest are the polymorphisms of interleukin-1 beta (IL-1b), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-a) genes and the factors that determine the production of these cytokines, since they play an important role in the pathophysiology of inflammation and in particular, in periodontal diseases. The identification of a specific IL-1 family genotype which correlates with the severity of periodontitis, demonstrates that it is genetic mechanisms that determine the intensity of immunoinflammatory response in different individuals (and hence, the severity of periodontal disease) due to the presence and persistence of bacterial plaque. This mini-review focuses on the current state of knowledge of genetic polymorphisms in patients with chronic periodontitis. Extensive studies on genetic factors in chronic periodontitis raise hopes for the identification of determinants related to disease susceptibility and improved diagnosis and treatment of chronic periodontitis, as well as prediction of disease progression.
Background: The understanding of the pathogenesis of periodontitis makes various progresses in the last decades. Today it is well known that the synthesis of high levels of pro-inflammatory mediators from gingival tissues in response to periodontopathogens results in destruction of soft and hard periodontal tissues and clinical expression of periodontal disease. There is enough evidence that PGE2 and IL-1beta are important mediators in the initiation and progression of periodontal disease. Detection of numerous cytokines in high levels in gingival tissues and crevicular fluid may be indicator for activity of periodontitis. The reduction of IL-1beta and PGE2 levels after periodontal therapy may be a potential criterion for successful periodontal therapy. The occurrence of increased IL-1beta and PGE2 levels in GCF or gingival tissue is able to indicate risk from progression of destruction in specific periodontital site. The current conception of the pathogenesis of periodontitis suggests that additional host modulation approach may inhibit the production of pro-inflammatory mediators in periodontal tissues and may enhance the treatment result. Aim of the study: To evaluate the effectiveness of additional host modulation therapy with NSAID (Aulin®) in non-surgical therapy of chronic periodontitis by measurement of IL-1beta and PGE2 gene expression levels in patient’s gingival tissues. Materials and methods: Evaluation of prostaglandin E2 (PGE2) and interleukin-1beta (IL-1beta) gene expression levels in gingival tissue of chronic periodontitis patients before and after non-surgical periodontal therapy (scaling and root planing) was performed. Prostaglandin E2 (PGE2) and interleukin-1beta (IL-1beta) gene expression levels in gingival tissue of patients with chronic periodontitis receiving conventional mechanical therapy alone or with additional host modulation therapy with NSAID (Aulin®) – 100 mg per day were compared. PCR analysis- TagMan RT-PCR for evaluation of gene expression levels of IL-1beta and PGE2 in gingival tissue of periodontal patients was applied. Results: Statistically significant differences were found between additional Aulin® therapy group and conventional therapy group. Received correlative coefficient with Spearman analysis was respectively t = -0.72 (p< 0,05) for IL-1beta and t = 0.81(p<0,05) for PGE2. The negative values of ddCt in test group reveal lower level of inhibition of gene expression. The comparative analysis of the collected data demonstrates fewer differences between both groups. The deviations in gene expression levels of IL -1beta and PGE2 are higher in the patients treated with adjunctive medication with Aulin®. Conclusion: This study confirms the effectiveness of non-surgical therapy in moderate and severe periodontitis. Additional use of non-steroidal anti-inflammatory agent Aulin® results in higher inhibition of the pro-inflammatory cytokines IL-1beta and PGE2. This data may be the base for modifying the conventional non-surgical therapy by including anti-inflammat...
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