Indigenous Microbiota Protects against Inflammation-Induced Osteonecrosis.

Medication-related osteonecrosis of the jaw (MRONJ) is a rare intraoral lesion that occurs in patients undergoing long-term and/or high-dose therapy with nitrogen-containing bisphosphonates, a RANKL inhibitor, antiangiogenic agents, or mTOR inhibitors. The presence of pathogenic bacteria is highly associated with advanced stages of MRONJ lesions; however, the exact role of indigenous microbes in MRONJ development is unknown. Here, we report that the normal oral flora in mice protects against inflammation-induced osteonecrosis. In mice that developed osteonecrosis following tooth extraction, there was increased bacterial infiltration when compared with healed controls. Antibiotic-mediated oral dysbiosis led to a local inhibition of bone resorption in the presence of ligature-induced periodontitis (LIP). There was no significant difference in empty lacunae, necrotic bone formation, osteoclast number, and surface area in antibiotic-treated as compared with conventionally colonized mice following extraction of healthy teeth after zoledronic acid infusions. However, extraction of LIP teeth led to increased empty lacunae, necrotic bone, and osteoclast surface area in antibiotic- and zoledronic acid-treated mice as compared with conventionally colonized mice. Our findings suggest that the presence of the indigenous microbiota protects against LIP-induced osteonecrosis.

N-acetyl cysteine protects pulp cells from resin toxins in vivo.

Potential risks of the use of resin-based restorative materials include direct damage to the pulp cells and the induction of hypersensitivity reactions in patients. In this study, we tested the hypothesis that N-acetyl cysteine (NAC) inhibits resin toxicity and restores the function of pulp cells. Analysis of our data demonstrates toxicity of composite resins on pulp cells in both an in vivo rat and an ex vivo human model system. Moreover, cells that survive after the placement of composites are weaker, and they are induced to undergo cell death when exposed to 2-hydroxyethyl methacrylate (HEMA). The toxic effect of composites on pulp cells is neutralized by NAC. Therefore, NAC protects the cells from damage induced by clinically relevant levels of restorative materials, in both rat and human model systems. The addition of N-acetyl cysteine prior to or concomitant with the application of restorative materials may be beneficial for the health and safety of dental patients.

Custom built bite-block endotracheal tube holder for prolonged intubation.

This case report describes an intensive care patient with recurrent endotracheal tube occlusion due to biting. The use and fabrication of a new form of custom built bite-block to resolve these problems is described. The device described may also provide better access for mouth care and simplify airway management compared with bite-blocks commonly used.

Detection of radiation-induced cervical atheromas by panoramic radiography.

Therapeutic irradiation of the neck is frequently used to treat patients with head and neck carcinoma. The irradiation, however, has been implicated as the cause of cervical carotid artery atherosclerotic lesions and subsequent stroke. Panoramic radiography previously shown capable of demonstrating isolated lesions was used to assess their development over time. Individuals with a pre-irradiation radiograph free of atheromas were enrolled for study. The prevalence rate of atheroma formation on post-irradiation (bilateral portals at >/=45 Gy) radiographs obtained at an interval of >/=36 months was determined. A control group of non-irradiated patients having similar risk factors for head and neck carcinoma and atherosclerosis and having an initial radiograph free of atheroma formation were likewise enrolled for study. The prevalence rate of atheroma formation on a second radiograph obtained from these individuals at an interval of >/=36 months was determined. The study population consisted of 17 patients, with a mean age of 56.5 (range 21.5-77.8) years who received a mean therapeutic irradiation dose of 53.2 Gy (range 45-71) to each side of their neck. The prevalence rate of atheromas manifested on the post-irradiation radiographs was 53%. These radiographs were obtained, on average, 69.7 (range 37-133) months after completion of radiation therapy. The prevalence rate of atheromas manifested on the second radiograph of patients in the control group was 5.9%. These radiographs were obtained, on average, 53.5 (range 52-55) months after the first. The difference in prevalence rates was statistically significant (p=0.0003). Individuals who have received therapeutic irradiation to the neck are more likely to develop carotid artery atheromas after treatment than are risk-matched control patients who have not been irradiated. These lesions can be detected by panoramic radiography.

Effect of carbamide peroxide bleaching on the shear bond strength of composite to dental bonding agent enhanced enamel.

STATEMENT OF PROBLEM: Carbamide peroxide bleaching has been implicated in adversely affecting the bond strength of composite to enamel. PURPOSE: This in vitro study evaluated the effect of 3 dental bonding agents (OptiBond, All-Bond 2, One-Step) on the shear bond strength of a hybrid composite to enamel which was treated by a 10% carbamide peroxide bleaching system. MATERIAL AND METHODS: Cylinders of composite were bonded to carbamide peroxide-treated enamel on extracted human teeth using 3 dental bonding agents. After thermocycling, shear bond strengths were determined with a universal testing machine. RESULTS: OptiBond aided bond strengths were 23.7 +/- 5.6 MPa to bleached and 19.6 +/- 2.9 MPa to unbleached enamel. For All-Bond 2, bleached enamel exhibited bond strengths of 14.9 +/- 4.0 MPa and unbleached enamel exhibited a bond strength value of 20. 4 +/- 2.3 MPa. The composite bond strength for One-Step was 13.6 +/- 5.9 MPa to bleached and 23.0 +/- 3.9 MPa to unbleached enamel. There was no statistical difference between OptiBond (alcohol base) aided bond strengths for bleached and unbleached enamel; however, the bond strength of composite to bleached enamel with All-Bond 2 or One-Step (acetone base) was significantly lower than unbleached controls. CONCLUSION: The effect of bonding agent usage on composite bond strength to enamel bleached with a particular carbamide peroxide was dependent on the bonding agent used.

The effect of chitosan (poly-N-acetyl glucosamine) on lingual hemostasis in heparinized rabbits.

PURPOSE: The purpose of this study was to evaluate the effect of chitosan on lingual hemostasis in rabbits whose coagulation pathway had been impaired by administration of intravenous heparin. MATERIALS AND METHODS: Bleeding times were measured for bilateral (15 mm x 2 mm) tongue incisions in 10 New Zealand white rabbits. Using a randomized, blinded experimental design, one incision in each animal was treated with chitosan, and the other was treated with the control vehicle without chitosan. Activated coagulation times and extraoral bleeding times were measured for each animal before, during, and after heparinization. RESULTS: Intravenous infusion of heparin more than tripled the mean activated coagulation time and increased mean systemic bleeding time by 40%. In this heparinized animal model, lingual incisions receiving the experimental substance showed a 43% improvement in bleeding time as compared with lingual incisions receiving the control solution (P< or =.001). Chitosan treatment brought bleeding time of the lingual incision for heparinized animals within the normal range. Scanning electron microscopic evaluation of the incisions treated with chitosan showed an altered red blood cell morphology and an unusual affinity between erythrocytes. CONCLUSIONS: Topical application of chitosan to lingual incisions effectively decreased intraoral bleeding time in a therapeutically anticoagulated (heparinized) rabbit model. Chitosan facilitated lingual hemostasis, possibly through interaction with erythrocytes, linking them together to establish a cellular clot or hemostatic plug.

Dental management of patients undergoing chemotherapy.

Of the increasing number of patients receiving chemotherapy, about 40 percent will develop significant oral problems during each exposure to the medication. Because of its rapid growth and cell turnover rate, the oral mucosa is very vulnerable to chemotherapy. Essentially all oral complications of the therapy occur through direct or indirect stomatotoxicity. The goal of care for this patient population is to maintain the integrity of the oral mucosa, prevent secondary infection, provide pain relief and maintain dietary intake.

Non-histone chromosomal protein HMG1 modulates the histone H1-induced condensation of DNA.

Circular dichroic spectra revealed that the previously known regular, asymmetric condensation of DNA by H1 histone was modulated by HMG1, a nonhistone chromosomal protein. Under approximately physiological salt and pH conditions (150 mM NaCl, pH 7), ellipticities at 270 nm were observed as follows: DNA, 9 X 10(3) degree, cm2/dmol nucleotide; DNA X H1 histone complex (1:0.4, w/w), -37 X 10(3) degree, cm2/dmol nucleotide, and DNA X H1 X HMG1 complex (1:0.4:0.4 w/w/w), -52 X 10(3) degree, cm2/dmol. HMG1 by itself did not distort the spectrum of DNA, showing that the effect of HMG1 on the DNA X H1 complex was not simply the summation of individual effects of HMG1 and H1 on the DNA spectrum. The effect of added HMG1 on the spectrum of the preformed DNA X H1 complex depended on the amount of HMG1 added and developed slowly (a day) as if a structure required annealing. The ternary complex, DNA X HMG1 X 1, seemed to represent a specific structure, since its formation depeNded on the reduced sulfhydryl state of HMG1; the disulfide form of HMG1, which was shown by circular dichroism to contain more random coil than did the reduced form, had no effect on the circular dichroic spectrum of the DNA X H1 complex.