Destruction Of Periodontal Ligament Research Articles

Development, in vitro and in vivo Evaluation of Novel Injectable Smart Gels of Azithromycin for Chronic Periodontitis

Periodontitis is an inflammatory condition affecting teeth resulting in progressive destruction of periodontal ligaments, resorption of alveolar bone and loss of teeth. Treatment of periodontitis includes surgical and non surgical management. Systemic antibiotics are also used for the treatment of periodontitis. The aim of this research was to formulate smart gel system of azithromycin (AZT) and to evaluate in vitro and in vivo for non-surgical treatment of chronic periodontitis. Azithromycin dihydrate, used systemically in the treatment of periodontitis, was formulated into smart gels using biodegradable, thermosensitive polymer Pluronic® F-127 (PF-127) and Hydroxy Ethyl Cellulose (HEC) as copolymer. The prepared smart gels were evaluated for sterility, content uniformity, gelation temperature and time, syringeability, rheological behavior, in vitro diffusion and in vivo efficacy in human patients. The prepared smart gels were clear and transparent, sterile, thermoresponsive and injectable. Viscosity of gels increased with increase in concentration of polymer/co-polymer and also with temperature. They gelled in short response time below the body temperature. In vitro release studies showed controlled drug release which was influenced significantly by the properties and concentration of PF-127 and HEC. In vivo efficacy studies showed a significant improvement (p <0.001) in clinical parameters such as gingival index, probing pocket depth, clinical attachment level, bleeding index and plaque index. The developed azithromycin smart gel system is a novel approach for the treatment of chronic periodontitis since it reduces the dose and side effects, bypasses the usual surgical procedures and improves patient compliance.

Periodontitis: A risk factor to respiratory diseases

Sir, Periodontitis is a destructive inflammatory disease of the supporting tissues of the teevth and is caused by specific microorganisms or group of specific microorganisms resulting in progressive destruction of periodontal ligament and alveolar bone with periodontal pocket formation, gingival recession or both.[12] The host responds to the periodontal infections with an array of events involving both innate and adaptive immunity. Periodontitis has been proposed as having an etiological or modulating role in cardiovascular and cerebrovascular disease, diabetes, respiratory disease and adverse pregnancy outcome and several mechanisms have been proposed to explain or support such theories. Oral lesions are indicators of disease progression and oral cavity can be a window to overall health.[3] Bacteria are the prime etiological agents in periodontal disease, and it is estimated that more than 500 different bacterial species are capable of colonizing the adult mouth[1] and the lesions of the oral cavity have an immense impact on the quality of life of patient with complex advance diseases.[3] Respiratory infectious diseases such as bacterial pneumonia and bronchitis are common and costly, especially in institutionalized and elderly inpatients. Respiratory infection is thought to rely in part on the aspiration of oropharyngeal flora into the lower respiratory tract and failure of host defense mechanisms to eliminate the contaminating bacteria, which then multiply to cause infection. It has been suggested that dental plaque may act as a reservoir of respiratory pathogens, especially in patients with periodontal disease.[4] Several mechanisms have been proposed to explain the potential role of oral bacteria in the pathogenesis of respiratory infection, which include the following: (1) aspiration of oral pathogens (such as Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, etc.) into the lung to cause infection; (2) periodontal disease-associated enzymes in saliva may modify mucosal surfaces to promote adhesion and colonization by respiratory pathogens, which are then aspirated into the lung; (3) periodontal disease-associated enzymes may destroy salivary pellicles on pathogenic bacteria to hinder their clearance from the mucosal surface; and (4) cytokines originating from periodontal tissues may alter respiratory epithelium to promote infection by respiratory pathogens.[5] In elderly patients living in chronic care facilities, the colonization of dental plaque by pulmonary pathogens is frequent. Notably, the overreaction of the inflammatory process that leads to destruction of connective tissue is present in both periodontal disease and emphysema. This overreaction may explain the association between periodontal disease and chronic obstructive pulmonary disease, the fourth leading cause of death in the United States; these findings underline the necessity for improving oral hygiene among patients who are at risk and those living in long-term care institutions.[6] Thus, it is concluded that lesions of oral cavity have an immense impact on the quality of life of patient with complex advanced diseases.[3] Oral diseases especially periodontitis should be treated on priority basis to maintain the overall health and to minimize the risk for systemic infections and diseases.

Neutrophil elastase is involved in the initial destruction of human periodontal ligament

It has been reported that noncollagenous proteins may provide mechanical strength to the periodontal ligament. Several proteolytic activities, including that of neutrophil elastase, are reported to increase significantly in periodontal disease. The aim of this study was to investigate the function of neutrophil elastase in the initial destruction of periodontal ligament at early stages of periodontal disease. The detection and identification of proteinases in chronic periodontitis and healthy periodontal ligament were examined by zymographic and zymo-Western analysis. The morphological changes of periodontal ligament, digested with or without authentic proteinases, were observed using scanning electron microscopy. Increases in neutrophil elastase, plasminogen, and matrix metalloproteinase-9 were detected in periodontal ligament from chronic periodontitis, compared with healthy periodontal ligament. Among these proteinases, only neutrophil elastase digested the intact noncollagenous proteins of periodontium. When human healthy periodontal ligament was directly digested by neutrophil elastase in an in vitro system, the morphological features were quite similar to that of the periodontal ligament in chronic periodontitis . In healthy periodontal ligament, the collagen fibrils are covered with noncollagenous proteins containing 110 kDa acidic glycoprotein, which was degraded initially by the neutrophil elastase. It was concluded that neutrophil elastase is involved in the degradation of noncollagenous protein-covered collagen fibrils in the early destructive stages of periodontal disease.

Gingival Tissue and Crevicular Fluid Co-operation in Adult Periodontitis

Activated matrix metalloproteinase-3 (MMP-3) can contribute to periodontal ligament destruction in adult periodontitis. Since MMP-3 has been reported to activate proMMP-8 and -9, it was speculated that gingival tissue fibroblast-derived MMP-3 might, in periodontitis, be responsible for activation of gingival crevicular fluid (GCF) neutrophil-derived proMMP-8 and -9. Immunohistochemistry disclosed MMP-3 in gingival fibroblasts in periodontitis. Cultured gingival fibroblasts released only pro-MMP-3 when stimulated with tumor necrosis factor-alpha. However, Western blot revealed partially activated MMP-3, MMP-8, and MMP-9 in periodontitis GCF. Active MMP-8 (p < 0.05) and MMP-9 (p < 0.05) correlated with the presence of active MMP-3. It seems that resident gingival fibroblasts produce pro-MMP-3 in GCF, where it becomes activated, probably by cathepsin G or elastase released by neutrophils. Active MMP-3 then activates neutrophil-derived pro-MMP-8 and -9. Different tissue compartments/cells exert co-operative actions in mutual local MMP activation cascades.

Inhibitory effects of incadronate on the progression of rat experimental periodontitis by porphyromonas gingivalis infection.

Incadronate (YM175, disodium cycloheptylaminomethylenediphosphonate monohydrate), a bisphosphonate, has been suggested to prevent the bone resorption associated with periodontitis by inhibiting osteoclast activity. The purpose of this study was to investigate the effect of incadronate in preventing periodontal destruction in rats with Porphyromonas gingivalis-induced periodontitis. Periodontitis was induced in 35 Wister rats by inoculating P. gingivalis into the oral cavity and feeding the rats a soft diet for 4 weeks. Incadronate or placebo was administered to the oral cavity of the rats 2 days per week for 2, 4, or 8 weeks. P. gingivalis infection resulted in destruction of the periodontal ligament, reduced bone density, and caused inflammatory cell migration. Radiographic, morphometric, and histological results showed that incadronate had the ability to increase the bone mineral density (quantum level score; cortex 518.9 [placebo 612.8]; sponge 579.8 [placebo 672.0]) and to prevent periodontal ligament destruction (width 0.16 mm [placebo 0.20 mm]; area 0.36 mm2 [placebo 0.54 mm2]) after 8 weeks' administration. Furthermore, the polymorphonuclear leukocyte (PMN) infiltration in gingival tissue was significantly decreased. These results showed that incadronate inhibits bone resorption and PMN migration in P. gingivalis-induced periodontitis.

Effects of TNFalpha and prostaglandin E2 on the expression of MMPs in human periodontal ligament fibroblasts.

Accumulating evidence indicates that TNFalpha plays an important role in the pathogenesis of periodontitis, but the effect of TNFalpha on the degradation of the periodontal ligament is not well understood. This study used reverse transcriptase-PCR to investigate the effects of TNFalpha on matrix metalloproteinase (MMP) mRNA expression in human periodontal ligament fibroblasts. TNFalpha increased MMP-1, MMP-3 and MMP-13 mRNA levels in both a time-dependent (0-24 h) and a dose-dependent (0.1-10 ng/ml) manner. TNFalpha also increased COX-2 mRNA levels. Because elevation of COX-2 mRNA levels enhances the production of prostaglandins, we therefore investigated whether endogenous prostaglandins are involved in the MMP mRNA expression that is enhanced by TNFalpha. Pretreatment with the selective COX-2 inhibitor, NS-398, increased MMP-13 mRNA levels, while prostaglandin E2 and dibutyryl cyclic AMP decreased MMP-13 mRNA levels. Neither MMP-1 nor MMP-3 mRNA levels were affected by these chemicals. These findings indicate that prostaglandin E2 has a lowering effect on TNFalpha-enhanced MMP-13 mRNA levels, and that this effect is dependent on cAMP. Our results suggest that TNFalpha participates in periodontal ligament destruction by stimulating the production of MMPs (MMP-1, MMP-3 and MMP-13), while endogenous prostaglandin E2 has a negative feedback role in TNFalpha-enhanced MMP-13 production.

Penurunan Kekuatan Tarik Rantai Elastomerik Sintetis pada Retraksi Kaninus

The synthetic elastomeric chain (S.E.C) is one of the current most popular orthodontic accessory. There are many variance brands, types and colours available at the dental market. The alternative funtion of the chain is facilitates canine retraction. S.E.C is applied by stretching it to a certain distance, so it would be able to produce a certain needed force strength. S.E.C is made of polymer polyurethane, which is not recognizable as an ideal elastic material. The polymer is subjected to change its utilization. Researchers had showed that the declining of S.E.C force strength depends on its brand type, colour and the length of the stretching force. Further, a S.E.C of the same brand, type and colour might not produce and deliver the same initial force strength. Research studies reported that the optimal force applied for retracting canine without generating the destruction of periodontal ligament ranges 55-300 g.

Consensus Report: Abscesses of the Periodontium

83 The following working definitions for these lesions were developed by the group: Gingival abscess. A localized purulent infection that involves the marginal gingiva or interdental papilla. Periodontal abscess. A localized purulent infection within the tissues adjacent to the periodontal pocket that may lead to the destruction of periodontal ligament and alveolar bone. Pericoronal abscess. A localized purulent infection within the tissue surrounding the crown of a partially erupted tooth.

Molecular epidemiology of oral treponemes associated with periodontal disease.

Periodontitis, a disease responsible for tooth loss worldwide, is characterized by chronic inflammation of the periodontium, eventually leading to destruction of periodontal ligaments and supporting alveolar bone. Spirochetes, identified by dark-field microscopy as being the most predominant bacteria in advanced lesions, are thought to play a causative role. Various spirochetal morphotypes were observed, but most of these morphotypes are as yet uncultivable. To assess the role of these organisms we designed oligonucleotide probes for the identification of both cultivable and so far uncultivable spirochetes in periodontitis patients. Subgingival plaque specimens taken from diseased sites (n = 200) and healthy control sites (n = 44) from 53 patients with rapidly progressive periodontitis (RPP) were submitted to direct in situ hybridization or dot blot hybridization after prior amplification with eubacterial primers. Spirochetes were found in all patients, but their distributions varied considerably. Parallel use of oligonucleotide probes specific for cultivable or so far uncultivable treponemes suggested the presence of novel yet unknown organisms at a high frequency. These uncultivable treponemes were visualized by fluorescence in situ hybridization, and their morphologies, sizes, and numbers could be estimated. All RPP patients included in this study harbored oral treponemes that represent either novel species, e.g., Treponema maltophilum, or uncultivable phylotypes. Therefore, it is necessary to include these organisms in etiologic considerations and to strengthen efforts to cultivate these as yet uncultivable treponemes.