MATERIALS AND METHODS: Sixty patients with one dry socket each, at University Dental Hospital Sharjah, were divided into three treatment groups based on their choice. In group I (n = 30), conventional treatment comprising of gentle socket curettage and saline irrigation was done. Group II (n = 15) dry sockets were treated with CGF and group III (n = 15) sockets were lased with LLLT. All dry socket patients were seen at day 0 for treatment and subsequently followed-up at 4, 7, 14, and 21 days. Pain score, perisocket inflammation, perisocket tenderness, and amount of granulation tissue formation were noted.
STATISTICAL ANALYSIS: Data were analyzed as mean values for each treatment group. Comparisons were made for statistical analysis within the group and among the three groups to rank the efficacy of treatment using one-way analysis of variance (ANOVA). Statistically significant difference is kept at p < 0.05.
RESULTS: Conventional treatment group I took more than 7 days to match the healing phase of group II CGF treated socket and group III LLLT irradiated socket (p = 0.001). When healing rate between CGF and LLLT are compared, LLLT group III showed a delay of 4 days compared with CGF in granulation tissue formation and pain control.
CONCLUSION: CGF treated socket was superior to LLLT in its ability to generate 75% granulation tissue and eliminate pain symptom by day 7 (p = 0.001).
MATERIALS AND METHODS: Intact pregnant rats were administered 1 mg/kg/day testosterone alone or in combination with flutamide, finasteride or anastrozole, subcutaneously on day-1 of pregnancy till day 3. The rats were sacrificed at day 4 of pregnancy, which was considered as the uterine receptivity period for determining the expression and distribution of connexin 26 and connexion 43 by immunohistochemistry and quantitative polymerase chain reaction, respectively.
RESULTS: Treatment with 1 mg/kg/day testosterone increased connexin 26 and decreased connexin 43 mRNA expression and protein distribution in the uterus of early pregnancy rats.
CONCLUSION: Changes in the uterine connexin 26 and connexin 43 expression by testosterone could disrupt embryo implantation, resulting in early pregnancy loss.
MATERIALS AND METHOD: Forty-five patients with dry socket were divided into two treatment groups. Group I dry socket patients (n = 30) received conventional treatment while group II patients (n = 15) were irradiated with LLLT at a setting of 200-mW, 6-J, continuous-wave mode using an R02 tipless handpiece (Fotona Er:YAG, Europe), on the buccal, lingual, and middle surfaces of the socket for 30 s from a delivery distance of 1 cm. Pain score and quantification of granulation tissue in the socket were recorded at 0, 4, and 7 days post-dry socket treatment.
RESULTS: Results showed that the LLLT-irradiated group II sockets showed a much lower VAS pain score of 1-2 as early as day 4, and a richer amount of granulation tissue compared to the conventional treated group I socket. The amount and rate of granulation tissue formation in the dry socket are inversely proportional to the pain score showing significant clinical effectiveness of LLLT on promoting the healing of the dry socket, with improvement in symptoms (P = .001). Conventionally treated dry sockets take at least 7 days to match the effective healing of an LLLT-irradiated dry socket.
CONCLUSION: LLLT irradiation influences biomodulation of dry socket healing by dampening inflammation, promoting vascularization, stimulating granulation, and controlling pain symptoms.
CLINICAL RELEVANCE: LLLT may be an additional effective tool for managing dry sockets in general dental practice.
RESULTS: An investigation on the adherence, invasion and intracellular survival of bacterial strains within the bovine aortic endothelial cell line (BAEC) were carried out. The potential vaccine strain, P. multocida B:2 GDH7, was significantly better (p ≤ 0.05) at adhering to and invading BAEC compared to its parent strain and to P. multocida B:2 JRMT12 and survived intracellularly 7 h post treatment, with a steady decline over time. A dual reporter plasmid, pSRGM, which enabled tracking of bacterial movement from the extracellular environment into the intracellular compartment of the mammalian cells, was subsequently transformed into P. multocida B:2 GDH7. Intracellular trafficking of the vaccine strain, P. multocida B:2 GDH7 was subsequently visualized by tracking the reporter proteins via confocal laser scanning microscopy (CLSM).
CONCLUSIONS: The ability of P. multocida B:2 GDH7 to model bactofection represents a possibility for this vaccine strain to be used as a delivery vehicle for DNA vaccine for future multivalent protection in cattle and buffaloes.
RESULTS: Differences in disease outcome provided an opportunity to investigate the role of T cell immunity to FIP determined by T cell subset proliferation after stimulation with different viral antigens. Reduced total white blood cell (WBC), lymphocyte and T cell counts in blood were observed during primary acute infection for all experimental groups including cats that survived without clinical FIP. Antiviral T cell responses during early primary infection were also similar between cats that developed FIP and cats remaining healthy. Recovery of antiviral T cell responses during the later phase of acute infection was observed in a subset of cats that survived longer or resisted disease compared to cats showing rapid disease progression. More robust T cell responses at terminal time points were observed in lymph nodes compared to blood in cats that developed FIP. Cats that survived primary infection were challenged a second time to pathogenic FIPV and tested for antiviral T cell responses over a four week period. Nine of ten rechallenged cats did not develop FIP or T cell depletion and all cats demonstrated antiviral T cell responses at multiple time points after rechallenge.
CONCLUSIONS: In summary, definitive adaptive T cell responses predictive of disease outcome were not detected during the early phase of primary FIPV infection. However emergence of antiviral T cell responses after a second exposure to FIPV, implicated cellular immunity in the control of FIPV infection and disease progression. Virus host interactions during very early stages of FIPV infection warrant further investigation to elucidate host resistance to FIP.