Achieving periodontal regeneration in class III furcation defects is challenging. Many studies have applied growth factors to periodontal defects, including fibroblast growth factors (FGFs), which demonstrate angiogenic activity and mitogenic ability. This study aimed to evaluate periodontal regeneration following the application of FGF-2 to deproteinized bovine bone mineral (DBBM) in surgically created supra-alveolar class III furcation defects of the mandibular premolars of beagles. The defects were divided into the control, DBBM, and FGF/DBBM groups. For the control group, only root planing was performed. For the DBBM group, only DBBM particles were implanted into the furcation. For the FGF/DBBM group, DBBM was soaked with 0.3% FGF-2 solution, and FGF-2/ DBBM was then positioned into the furcation. After 8 weeks, the dogs were euthanized. The micro-computed tomography analysis revealed that the changes in the bone volume of the furcation area were significantly greater in the FGF/DBBM group than in the DBBM group. In the histomorphometric analysis, the area of the newly formed bone was significantly greater in the FGF/DBBM group than in the DBBM or control group. The cementum extension was significantly longer in the FGF/DBBM or DBBM group than in the control group. The epithelial area was significantly less in the FGF/DBBM group than in the DBBM or control group. The application of FGF combined with DBBM to a class III defect enhanced the regeneration of periodontal tissues and increased the healing rate. This finding indicates that FGF-2 combined with DBBM can be applied to class III defects clinically.

BACKGROUND: Steroid acne have similar clinical manifestations with Malassezia folliculitis, so it is not easy to distinguish between these disease entities clinically. And there have been few reports about them and the therapeutic efficacy of antifungal agent for steroid acne. OBJECTIVE: We aimed to find out different points clinically between steroid-using acneiform eruption group and the group without use, and describe the results of direct-microscopic examinations and establish the relationships between therapeutic responses to oral antifungal agent and some variables like use of corticosteroids, grade of direct-microscopically positive score. METHODS: With 91 patients according to the protocol prepared, we described characteristics of the lesions, sites, and distributions, use of corticosteroids, then examined Malassezia spores with 10% KOH/Parker blue black ink mount from patient's skin lesions. And finally we compared the reponses to antifungal agent. For objective evaluation we used direct microscopic grading method to count spores introduced by Jacinto-Jamora et al. RESULTS: In both groups with and without use of corticosteroids, most had characteristics of papules and pustules, symmetric distributions except the patients using topical corticosteroids. In all positive groups, there was no significant difference in therapeutic responses regardless of the previous use of corticosteroids. Interestingly therapeutic response rate of (1+) group to itraconazole are similar with that of higher scoring groups. CONCLUSION: We suggest that not in a tropical area like Korea, direct-microscopically low score ((1+) or (2+)) and even negatives with typical manifestations of Malassezia folliculitis has a clinical significance and both steroid acne and Malassezia folliculitis may be one spectrum of the same disease.
Acne Vulgaris* ; Acneiform Eruptions ; Adrenal Cortex Hormones ; Folliculitis* ; Humans ; Ink ; Itraconazole ; Korea ; Malassezia* ; Skin ; Spores

BACKGROUND: Analgesic tolerance to opioids has been described in both experimental and clinical conditions, which may limit their clinical utility. This study investigated the effects of intrathecal adenosine A1 receptor agonist (R-PIA) on spinal morphine tolerance. METHODS: SD rats were given intrathecal injections of saline 10microliter, R-PIA 10microgram, morphine 10microgram, or R-PIA plus morphine combinations for 7 days (R-PIA given for days 1-7; days 1-3; or days 5-7). Antiallodynic testing using von Frey filaments was carried out before and 30 minutes after the drug injection. On day 8, an antiallodynic dose-response curve was constructed and the 50% effective dose (ED(50)) for morphine (given alone) was calculated for each study group. RESULTS: The coinjection group of R-PIA with morphine blocked the development of tolerance, as shown by the preservation of morphine antiallodynia over 7 days the concomitant decrease in the ED(50) values on day 8, compared with the morphine-alone group. Although additive analgesia over days 1-7 cannot be ruled out, the reductions of the ED(50) in the R-PIA and morphine combination group suggest some suppression of tolerance. CONCLUSIONS: These results suggest that intrathecal R-PIA prevents the development of spinal opioid tolerance. Future studies will be needed to examine the respective roles of supraspinal and peripheral sites of R-PIA and morphine interaction, and to investigate the mechanisms underlying the action of R-PIA on opioid tolerance.
Adenosine A1 Receptor Agonists* ; Adenosine* ; Analgesia ; Analgesics, Opioid ; Animals ; Hyperalgesia ; Injections, Spinal ; Models, Animal* ; Morphine* ; Pain, Postoperative* ; Rats* ; Receptor, Adenosine A1*

BACKGROUND: Alopecia areata usually has a complete recovery rate in most patients, but others eventually develop the severe chronic form. Unfortunately, its course and response rates are variable and unpredictable. OBJECTIVE: To identify patient and treatment factors predictive of therapeutic success and to develop a practical model for predicting patient response. METHODS: The medical records of 189 patients with alopecia areata from 1998 to 2001 at the Department of Dermatology, Chungnam National university hospital were reviewed. Most patients were treated by corticosteroids (topical, intralesional, and systemic). RESULTS: Variables independently associated with clinically significant regrowth were the duration between initiation of therapy, baseline extent of alopecia areata. 1. Both partial response and no response (PR+NR): long duration between initiation of therapy (>3month; especially >12 months), baseline extent of alopecia areata (>25%; especially 100%- alopecia totalis and universalis) and male patients. 2. Duration between initiation of therapy: Cosmetically acceptable hair regrowth was obtained in 6% of patients over 12 months, 57% with 4 to 12 months and 97% 0 to 3 months. So, it is better to start treating within 3 months; and at least within 12 months. 3. Baseline extent of alopecia areata: Cosmetically acceptable hair regrowth was obtained in 27% of patients with alopecia totalis/universalis, 64% with 26 to 99%, and 94% with below 25% alopecia areata. So, it showed a good response when below 25 %, but a poor response at above 25%, specially for 100%. CONCLUSION: These findings suggest that when the duration between initiation of therapy (>12 months) and the baseline extent of alopecia areata increases, the therapeutic effect decreases. A predictive model (decision tree) has been developed to assist with patient prognostication and counseling.
Male ; Humans ; Predictive Value of Tests

BACKGROUND: Even though the cause of atopic dermatitis is still unknown, it is considered an allergic reaction whose onset is frequently and strongly associated with both hereditary and environmental factors. The multiple allergosorbent test-chemiluminescent assay(MAST-CLA) is a new assay for serum allergen-specific IgE, and allows up to 35 allergens to be tested simultaneously. Furthermore, the MAST-CLA has shown good sensitivity, specificity, and a correlation with the RAST and skin prick test. OBJECTIVE: The purpose of this study was to find total IgE and allergen-specific IgE and to evaluate the correlations between clinical status and abnormal immunologic findings in MAST-CLA on atopic dermatitis patients. METHODS: Our study was designed by analyzing outpatients with atopic dermatitis via physical examination, questionnaires and the MAST-CLA with a total IgE and 35 allergen-specific IgE in 100 patients. RESULTS: The results were as follows; 1. Among the subjects(mean age=11.6 years, mean age of onset=28.7 months olds), 87% of patients showed elevated serum total IgE levels(more than class level 2) and 72% revealed at least more than one allergen-specific IgE by MAST-CLA. 2. The positive allergens rate, in descending order, were D. farinae 58%, D. pteronyssynus 54%, house dust 43%(aeroallergens), egg white 31%, milk 30%, and crab 22%(food allergens). 3. Good correlation was obtained between total IgE levels and number of positive allergen-specific IgE in MAST-CLA, with 0.497 correlation coefficient(p<0.05). The relationship between the clinical severity(SCORAD scores) and total IgE and allergen-specific IgE did not show statistical significance. 4. While age was significantly increased to positive of total IgE, over 12 year-old group was the highest(100%)(p<0.05). The highest rate of positive allergen-specific IgE was shown in the 7-12 year-old group(9.2+/-9.6), the difference of other groups was statistically significant(p<0.05). The relation of clinical status and result of MAST-CLA did not show statistical significancy but also correlation coefficient was low. 5. The 0-2 year-old group showed only food allergens and no aeroallergens, the positive rate of aeroallergens were 3-6 year-old group 80.2%, 7-12 years group 63.5%, over 12 years old group 73.7%. 6. Both total IgE level and allergen-specific IgE were significantly increased in patient groups with atopic personal history(p<0.05). But, there was not a significant difference in patient groups with or without family history. Also, the relationship among the clinical status, total IgE level, and number of positive allergen-specific IgE in patient groups with or without atopic personal or family history did not show significant difference(p>0.05). CONCLUSION: Our data suggested that MAST-CLA is a sensible and useful method to investigate the causative allergen-specific IgE and to evaluate in patients with atopic dermatitis with additional benefit of a non-isotopic technique and therefore not very expensive
Allergens ; Child ; Dermatitis, Atopic* ; Dust ; Egg White ; Humans ; Hypersensitivity ; Immunoglobulin E* ; Milk ; Outpatients ; Physical Examination ; Sensitivity and Specificity ; Skin ; Surveys and Questionnaires

Background: Atopic dermatitis (AD) is characterized by chronic, relapsing skin inflammation (eczema) with itchy sensation. Keratinocytes, which are located at the outermost part of our body, are supposed to play important roles at the early phase of type 2 inflammation including AD pathogenesis. Objective: The purpose of this study was to evaluate whether keratinocytes-derived reactive oxygen species (ROS) could be produced by the allergens or non-allergens, and the keratinocytes-derived ROS could modulate a set of biomarkers for type 2 inflammation of the skin. Methods: Normal human epidermal keratinocytes (NHEKs) were treated with an allergen of house dust mites (HDM) or a non-allergen of compound 48/80 (C48/80). Then, biomarkers for type 2 inflammation of the skin including those for neurogenic inflammation were checked by reverse transcriptase-polymerase chain reaction and western immunoblot experiments. Results: HDM or C48/80 was found to upregulate expression levels of our tested biomarkers, including type 2 T helper-driving pathway (KLK5, PAR2, and NF κ B), epithelial-cell-derived cytokines (thymic stromal lymphopoietin, interleukin [IL]-25, IL-33), and neurogenic inflammation (NGF, CGRP). The HDMor C-48/80-induced expression levels of the biomarkers could be blocked by an antioxidant treatment with 5 mM N-acetyl-cysteine. In contrast, pro-oxidant treatment with 1 mM H2O2 could upregulate expression levels of the tested biomarkers in NHEKs. Conclusion Our results reveal that keratinocytes-derived ROS, irrespective to their origins from allergens or non-allergens, have a potential to induce type 2 inflammation of AD skin.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.

Purpose: This study elucidates the mechanism of the physiological effect of cannabidiol (CBD) by assessing its impact on lipopolysaccharide (LPS)-induced inflammation in RWPE-1 cells and prostatitis-induced by 17β-estradiol and dihydrotestosterone in a rat model, focusing on its therapeutic potential for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). Materials and Methods: RWPE-1 cells were stratified in vitro into three groups: (1) controls, (2) cells with LPS-induced inflammation, and (3) cells with LPS-induced inflammation and treated with CBD. Enzyme-linked immunosorbent assays and western blots were performed on cellular components and supernatants after administration of CBD. Five groups of six Sprague–Dawley male rats were assigned: (1) control, (2) CP/CPPS, (3) CP/CPPS and treated with 50 mg/kg CBD, (4) CP/CPPS and treated with 100 mg/kg CBD, and (5) CP/CPPS and treated with 150 mg/kg CBD. Prostatitis was induced through administration of 17β-estradiol and dihydrotestosterone. After four weeks of CBD treatment, a pain index was evaluated, and prostate tissue was collected for subsequent histologic examination and western blot analysis. Results: CBD demonstrated efficacy in vivo for CP/CPPS and in vitro for inflammation. It inhibited the toll-like receptor 4 (TLR4)uclear factor-kappa B (NF-κB) pathway by activating the CB2 receptor, reducing expression of interleukin-6, tumor necrosis factor-alpha, and cyclooxygenase-2 (COX2) (p<0.01). CBD exhibited analgesic effects by activating and desensitizing the TRPV1 receptor. Conclusions CBD inhibits the TLR4/NF-κB pathway by activating the CB2 receptor, desensitizes the TRPV1 receptor, and decreases the release of COX2. This results in relief of inflammation and pain in patients with CP/CPPS, indicating CBD as a potential treatment for CP/CPPS.