Use of salivary biomarkers for diagnosis of periodontal disease activity: a literature review

Periodontal disease is an infectious disease characterized by the connective tissue destruction and consequent alveolar bone loss in response to plaque accumulation on the tooth surface. The clinical diagnosis of periodontal disease is based both on clinical examination involving the evaluation of probing depth and radiographic examination of alveolar bone loss but these examinations are not enough to determine the activity of the disease process. For that reason, it has been proposed to seek predictive disease markers in an attempt to assess the disease activity and so, evaluate the efficacy of the periodontal disease treatment. The aim of this review is to present recent advances in the development of proteomic, genomics and microbial biomarkers and potential clinical applications. It was concluded that periodontal treatment based on assessing the levels of salivary biomarkers emerges as a promising method in near future and will become an integral part of the evaluation of periodontal health.

Detecção de Periodontopatógenos, Glicoproteína Emmprin (Cd-147) e sua correlação com MMP-2 e MMP-9

Periodontitis is an infectious disease characterized by the secretion of a variety of inflammatory mediators that lead to destruction of tooth supporting tissues, including the possible loss of alveolar bone, in association with infection with multiple species of bacteria. It is estimated that more than 400 species colonize the biofilm and some oral species related to periodontal disease is present in the subgingival including P. gingivalis, T. forsythia and T. denticola. However, other organisms may be related of this disease, as Filifactor allocis and Prevotella tannerae. These microorganisms and subproducts such as endotoxins released into the extracellular lead to the stimulation of metalloproteinase inducer glycoprotein (EMMPRIN, CD-147), which stimulates the release of MMPs by host cells, like fibroblasts and endothelial cells, thus leading to tissue destruction. The objective of this study was to detect F. allocis, P. tannerae, T. denticola and the glycoprotein EMMPRIN (CD-147) and its correlation with MMP-2 and MMP-9 in subgingival fluid samples of patients with chronic periodontitis. Fluids were collected from healthy and disease subgingival sites of 20 healthy individuals before basic periodontal treatment and after of 60 days of treatment. Their DNAs were extracted and portions of the 16S gene were amplified and performed conventional PCR. For immunological analysis and quantification of EMMPRIN (CD-147), MMP-2 and MMP-9 was used ELISA-Sandwich. Results demonstrated that the disease group showed significantly high amounts of T. denticola, F. alocis and P. tannerae when compared with health sites. MMP-2 and MMP-9 were detected in high concentrations with statistically significantly reduction after periodontal treatment to MMP-2, but without correlation with EMMPRIN.

Long-term evaluation of oral gavage with periodontopathogens or ligature induction of experimental periodontal disease in mice

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Periodontite ulcerativa necrosante: tratamento fisico da superficie radicular com Er YAG laser

Necrotizing ulcerative periodontitis is associated with bacteria and predisposing risk factors. The treatment is centered in elimination and/or control of the bacteria and predisposing risk factors. However the disease acute phase could induce sequelae as periodontal tissue destruction which may be treated by periodontal surgical procedures.

Terpinen-4-ol: estudo do efeito sinérgico/aditivo, adesão em co-cultura e alteração dos fatores de virulência sobre Candida spp

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Inflamassomos NLRC4 E NLRP3 na Doença Periodontal Experimental Induzida por Aggregatibacter Actinomycetemcomitans

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Role of periodontal pathogenic bacteria in RANKL-mediated bone destruction in periodontal disease

Accumulated lines of evidence suggest that hyperimmune responses to periodontal bacteria result in the destruction of periodontal connective tissue and alveolar bone. The etiological roles of periodontal bacteria in the onset and progression of periodontal disease (PD) are well documented. However, the mechanism underlying the engagement of periodontal bacteria in RANKL-mediated alveolar bone resorption remains unclear. Therefore, this review article addresses three critical subjects. First, we discuss earlier studies of immune intervention, ultimately leading to the identification of bacteria-reactive lymphocytes as the cellular source of osteoclast-induction factor lymphokine (now called RANKL) in the context of periodontal bone resorption. Next, we consider (1) the effects of periodontal bacteria on RANKL production from a variety of adaptive immune effector cells, as well as fibroblasts, in inflamed periodontal tissue and (2) the bifunctional roles (upregulation vs. downregulation) of LPS produced from periodontal bacteria in a RANKL-induced osteoclast-signal pathway. Future studies in these two areas could lead to new therapeutic approaches for the management of PD by down-modulating RANKL production and/or RANKL-mediated osteoclastogenesis in the context of host immune responses against periodontal pathogenic bacteria. © 2010 Mikihito Kajiya et al.