H. Xiong

Effect of alendronate on alveolar bone resorption and angiogenesis in rats with experimental periapical lesions

AIM To investigate the effects of systemically administered alendronate, one of the most potent bisphosphonates (BPs), on alveolar bone resorption and angiogenesis in rats subjected to experimental periapical lesions over two time periods. METHODOLOGY Forty adult Sprague-Dawley (SD) rats were divided equally into control and experimental groups, and the pulp chambers of mandibular first molars of all rats were exposed to the oral environment to induce periapical lesions. The experimental group received daily subcutaneous injections of alendronate at a dose of 0.25 mg kg(-1), whereas the control group received only the saline vehicle. These injections were initiated 1 week before the periapical lesion induction and then continued daily throughout the entire experimental period. After 2 or 4 weeks following pulp exposure, the rats were killed, and the mandibles were examined histologically for periapical bone loss area, number of microvascular vessels (NMV) and tartrate-resistant acid phosphatase (TRAP) activity. RESULTS Overall, periapical bone loss area and the number of TRAP-positive cells (osteoclasts) were significantly decreased at 2 and 4 weeks, respectively, after daily subcutaneous injection of alendronate compared with the control group (P < 0.05). There was no significant decrease change in NMV (P > 0.05). CONCLUSIONS Administration of alendronate to rats might inhibit alveolar bone resorption associated with periapical disease, which might not lead to impairment of angiogenesis. However, because of the differences between rats and humans, one has to consider the possible consequences of this treatment in the clinic.

Boundary-Lubricating Ability and Lubricin in Synovial Fluid of Patients With Temporomandibular Joint Disorders

PURPOSE This study was conducted to measure the boundary-lubricating ability and lubricin concentration of synovial fluid (SF) from patients with different stages of temporomandibular joint disorders (TMDs) and establish relationships between them. PATIENTS AND METHODS According to the imaging and clinical findings, TMD patients were divided into 3 subgroups: displaced disc with reduction, displaced disc without reduction, and osteoarthritis. The boundary-lubricating ability of SF was determined by the coefficient of friction (COF) of SF in vitro with a friction apparatus. The lubricin concentrations were quantified by enzyme-linked immunosorbent assays. RESULTS The COF of SF in TMD patients was significantly higher than that of healthy control subjects, but no observed difference was found among patient subgroups. Furthermore, a significant decline in lubricin concentrations was found in the group with osteoarthritis, whereas there was no significant change in the other groups. However, a significant correlation was not found between the COF and the lubricin concentrations in our study. CONCLUSIONS These findings showed that distinct changes in lubricin and boundary-lubricating ability in the SF occurred with different stages of TMDs.

IL-17 stimulates the production of the inflammatory chemokines IL-6 and IL-8 in human dental pulp fibroblasts

AIM To investigate IL-17 expression in human pulpitis and to study the effects of IL-17 on the secretion of the chemokines IL-6 and IL-8 and the related signalling pathways. METHODOLOGY Samples of human dental pulp tissue were obtained from healthy controls and patients with pulpitis. Cytokine IL-17 messenger RNA (mRNA) expression in the pulp tissue was detected by real-time polymerase chain reaction. In addition, human dental pulp fibroblasts (HDPFs) were stimulated with IL-17. Production of IL-6 and IL-8 was determined by reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assay. Aspects of the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs) signalling pathways were examined by Western blot analysis. RESULT Increased levels of IL-17 mRNA were found in inflamed dental pulp tissue (pulpitis). Stimulation of dental pulp tissue with IL-17 induced the production of IL-6 and IL-8 in a dose-dependent manner. In addition, IL-17 stimulation resulted in rapid activation of nuclear factor-kappaB (NF-κB), phosphorylation of p38 MAPK, extracellular signal-regulated kinase (ERK) and Jun N-terminal kinase (JNK) in HDPFs. CONCLUSION IL-17 may participate in pulp tissue inflammation through chemokine production and NF-κB and MAPKs signalling pathways.

Expression of a cytokine, interleukin-23, in experimental periapical lesions.

AIM To investigate the expression of interleukin (IL)-23, a new member of the IL-12 family, in experimental periapical lesions. METHODOLOGY Periapical lesions were induced in Wistar rats by occlusal surface pulp exposure in mandibular first molars. The rats were randomly sacrificed 0, 7, 14, 21, 28, 35, 42 and 56 days after pulp exposure. The jaws that contained the first molars were obtained and routinely prepared for radiographic, histological, enzyme histochemical, immunohistochemical and double immunofluorescence analyses. Data were analysed by one-way analysis of variance and the Pearson correlation test. RESULTS The number of IL-23-positive cells increased from day 7 to day 35 and then gradually decreased. The number of osteoclasts increased and peaked on day 14 and then gradually decreased from day 21 to day 56. A significant positive correlation existed between the number of IL-23 positive cells and the size of bone resorption in periapical lesions from day 7 to day 56 (r = 0.875, P < 0.01). CONCLUSIONS Interleukin-23 can be observed and may be associated with inflammatory response and bone resorption in periapical lesions.

The involvement of Platelet‐derived growth factor‐A in the course of apical periodontitis

AIM To investigate the expression of platelet-derived growth factor-A (PDGF-A) in the course of apical periodontitis induced in rats and to explore its possible role in the development of periapical lesions. METHODOLOGY Apical periodontitis was induced in SD rats by exposing the pulp of mandibular first molars to the oral environment for 0-42 days. Animals were killed at 0, 7, 14, 21, 28 and 42 days after lesion induction. The development of periapical lesions was investigated by radiographic and histochemical examination. Changes in the level and distribution of PDGF-A in the periapical tissue were examined by immunohistochemistry. The radiographs were scanned to a computer, and the areas of periapical lesions were calculated. Osteoclasts and PDGF-A-positive cells were counted in five randomly selected areas in each specimen. The data were then analysed by one-way ANOVA using the SPSS 13.0 statistical package. RESULTS The lesions expanded from day 0 to day 21 and stabilized thereafter. PDGF-A-positive cells were observed in the periapical tissue from 7 day postoperatively. Between 7 and 21 days, when expansion of the periapical lesion was most evident, numerous PDGF-A-positive cells were found in the periapical tissue. The number of these cells showed further increases at 28 and 42 days postoperatively. Many of the PDGF-A-positive cells were inflammatory cells with different morphologies. The variation tendency of the number of PDGF-A-positive cells per high-power field was similar to that areas of the periapical lesions. CONCLUSIONS Platelet-derived growth factor-A might be involved in the development of periapical lesions.