BackgroundThe aim of the study was to evaluate the knowledge of ER physicians with different specialties, experience and hospital sectors for the management of avulsed teeth in the emergency rooms of eight major hospitals in Jeddah, Saudi Arabia. It also covers their attitude towards receiving further education on tooth avulsion management.MethodsA cross-sectional survey was conducted at the emergency rooms of eight hospitals in Jeddah from August to December 2015. A self-administered questionnaire consisting of 31 multiple choice questions assessing both knowledge and attitude was distributed to 150 physicians who were working in the ER departments.ResultsResponse rate was 81.33%. Data revealed that 45.9% of the respondents did not have prior knowledge about avulsion. Physicians working in military hospitals had better knowledge about the ER management of avulsion cases than physicians of public hospitals. 80.3% of participants showed willingness to replant the tooth, however, 65.3% would not do it by themselves. 42.6% of the physicians did not know the importance of extra-oral time. Milk was selected as the best transport media for avulsed tooth by 31.1% of the participants. Regarding physicians’ attitude, 95.1% showed interest in receiving information about the subject.ConclusionThis study revealed that the majority of ER physicians lack the knowledge needed to manage avulsions cases. Hence, educational programs are necessary for ER physicians to provide proper management for those cases.Electronic supplementary materialThe online version of this article (10.1186/s12903-018-0515-5) contains supplementary material, which is available to authorized users.

Steroidal dexamethasone is as effective as non-steroidal ibuprofen for preventing or controlling postoperative pain and discomfort after surgical implant placement.

By binding to its chemokine receptor CXCR4 on osteoclast precursor cells (OCPs), it is well known that stromal cell-derived factor-1 (SDF-1) promotes the chemotactic recruitment of circulating OCPs to the homeostatic bone remodeling site. However, the engagement of circulating OCPs in pathogenic bone resorption remains to be elucidated. The present study investigated a possible chemoattractant role of macrophage migration inhibitory factor (MIF), another ligand for C-X-C chemokine receptor type 4 (CXCR4), in the recruitment of circulating OCPs to the bone lytic lesion. To accomplish this, we used Csf1r-eGFP-knock-in (KI) mice to establish an animal model of polymethylmethacrylate (PMMA) particle-induced calvarial osteolysis. In the circulating Csf1r-eGFPþ cells of healthy Csf1r-eGFP-KI mice, Csf1rþ/CD11bþ cells showed a greater degree of RANKL-induced osteoclastogenesis compared to a subset of Csf1rþ/RANKþ cells in vitro. Therefore, Csf1r-eGFPþ/CD11bþ cells were targeted as functionally relevant OCPs in the present study. Although expression of the two cognate receptors for MIF, CXCR2 and CXCR4, was elevated on Csf1rþ/CD11bþ cells, transmigration of OCPs toward recombinant MIF in vitro was facilitated by ligation with CXCR4, but not CXCR2. Meanwhile, the level of PMMA-induced bone resorption in calvaria was markedly greater in wild-type (WT) mice compared to that detected in MIF-knockout (KO) mice. Interestingly, in contrast to the elevated MIF, diminished SDF-1 was detected in a particle-induced bone lytic lesion of WT mice in conjunction with an increased number of infiltrating CXCR4þ OCPs. However, such diminished SDF-1 was not found in the PMMA-injected calvaria of MIF-KO mice. Furthermore, stimulation of osteoblasts with MIF in vitro suppressed their production of SDF-1, suggesting that MIF can downmodulate SDF-1 production in bone tissue. Systemically administered anti-MIF neutralizing monoclonal antibody (mAb) inhibited the homing of CXCR4þ OCPs, as well as bone resorption, in the PMMA-injected calvaria, while increasing locally produced SDF-1. Collectively, these data suggest that locally produced MIF in the inflammatory bone lytic site is engaged in the chemoattraction of circulating CXCR4þ OCPs.

Locally produced osteoclastogenic factor RANKL plays a critical role in the development of bone resorption in periradicular periodontitis. However, because RANKL is also required for healthy bone remodeling, it is plausible that a costimulatory molecule that upregulates RANKL production in inflammatory periradicular periodontitis may be involved in the pathogenic bone loss processes. We hypothesized that macrophage migration inhibitory factor (MIF) would play a role in upregulating the RANKL-mediated osteoclastogenesis in the periradicular lesion. In response to pulp exposure, the bone loss and level of MIF mRNA increased in the periradicular periodontitis, which peaked at 14 d, in conjunction with the upregulated expressions of mRNAs for RANKL, proinflammatory cytokines (TNF-a, IL-6, and IL-1b), chemokines (MCP-1 and SDF-1), and MIF's cognate receptors CXCR4 and CD74. Furthermore, expressions of those mRNAs were found significantly higher in wild-type mice compared with that of MIF 2/2 mice. In contrast, bacterial LPS elicited the production of MIF from ligament fibroblasts in vitro, which, in turn, enhanced their productions of RANKL and TNF-a. rMIF significantly upregulated the number of TRAP + osteoclasts in vitro. Finally, periapical bone loss induced in wild-type mice were significantly diminished in MIF 2/2 mice. Altogether, the current study demonstrated that MIF appeared to function as a key costimulatory molecule to upregulate RANKL-mediated osteoclastogenesis, leading to the pathogenically augmented bone resorption in periradicular lesions. These data also suggest that the approach to neutralize MIF activity may lead to the development of a therapeutic regimen for the prevention of pathogenic bone loss in periradicular periodontitis.

Apical periodontitis (periapical lesions) is an infection-induced chronic inflammation in the jaw, ultimately resulting in the destruction of apical periodontal tissue. Toll-like receptors (TLRs) are prominent in the initial recognition of pathogens. Our previous study showed that TLR4 signaling is proinflammatory in periapical lesions induced by a polymicrobial endodontic infection. In contrast, the functional role of TLR2 in regulation of periapical tissue destruction is still not fully understood. Using TLR2 deficient (KO), TLR2/TLR4 double deficient (dKO), and wild-type (WT) mice, we demonstrate that TLR2 KO mice are highly responsive to polymicrobial infection-induced periapical lesion caused by over activation of TLR4 signal transduction pathway that resulted in elevation of NF-κB (nuclear factor kappa B) and proinflammatory cytokine production. The altered TLR4 signaling is caused by TLR2 deficiency-dependent elevation of CD14 (cluster of differentiation 14), which is a co-receptor of TLR4. Indeed, neutralization of CD14 strikingly suppresses TLR2 deficiency-dependent inflammation and tissue destruction in vitro and in vivo. Our findings suggest that a network of TLR2, TLR4, and CD14 is a key factor in regulation of polymicrobial dentoalveolar infection and subsequent tissue destruction.