scholarly journals Decompression Effects on Suppurative and Sclerosing Osteomyelitis in the Jaw

Author(s):  
Buyanbileg Sodnom-Ish ◽  
Mi Young Eo ◽  
Ji Hye Oh ◽  
Mi Hyun Seo ◽  
Hoon Joo Yang ◽  
...  

Abstract Background: Osteomyelitis (OM) of the jaw is usually caused by a chronic odontogenic infection. Decompression is the release the intraluminal pressure in the cystic cavity allowing gradual bone growth from the periphery. The aim of this study was to analyze the effectiveness of decompression in an OM jaw model.Methods: A 4-mm-diameter defect was made on mandibles of fourteen Sprague-Dawley rats and inoculated with S. aureus (20 μl of 1x107 CFU/ml) injection. Two weeks later, four groups were made as non-treatment (C1), only curettage (C2), curettage and decompression (E1), and curettage and decompression with normal saline irrigation (E2). After four weeks, each group was analyzed.Results: Most micro-CT parameters of C1 and C2 were significantly lower, and bone mineral density with bone volume was enhanced in E2. E1 and E2 groups in histology showed prominent bone healing with a significantly high number of osteocytes, E2 had the weakest expression of IL-6 compared to that of C1. TNF-α and OPN were expressed strongly in the E1.Conclusion: Decompression drains induced advanced bone healing compared to that of curettage alone in an OM jaw model. Therefore, it could be recommended to use decompressive drain for the enhancement of jaw OM management.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Buyanbileg Sodnom-Ish ◽  
Mi Young Eo ◽  
Ji Hye Oh ◽  
Mi Hyun Seo ◽  
Hoon Joo Yang ◽  
...  

AbstractOsteomyelitis (OM) of the jaw is usually caused by a chronic odontogenic infection. Decompression is the release the intraluminal pressure in the cystic cavity allowing gradual bone growth from the periphery. The aim of this study was to analyze the effectiveness of decompression in an OM jaw model. A 4-mm-diameter defect was made on mandibles of fourteen Sprague–Dawley rats and inoculated with S. aureus (20 μl of 1 × 107 CFU/ml) injection. Two weeks later, four groups were made as non-treatment (C1), only curettage (C2), curettage and decompression (E1), and curettage and decompression with normal saline irrigation (E2). After four weeks, each group was analyzed. Most micro-CT parameters, including bone mineral density [0.87 (± 0.08) g/cm3] with bone volume [0.73 (± 0.08) mm3] was higher in E2 group than that of C1 group (p = 0.04, p = 0.05, respectively). E2 group in histology showed the highest number of osteocytes than those of control groups, 91.00 (± 9.90) (p = 0.002). OPN were expressed strongly in the E1 (“5”: 76–100%) that those of other groups. Decompression drains induced advanced bone healing compared to that of curettage alone. Therefore, it could be recommended to use decompressive drain for enhancing the jaw OM management.


1974 ◽  
Vol 75 (4) ◽  
pp. 669-682 ◽  
Author(s):  
K.-G. Thorngren ◽  
L. I. Hansson

ABSTRACT The growth stimulating effect of growth hormone was determined with tetracycline as intravital marker of the longitudinal bone growth of proximal tibia in female Sprague-Dawley rats hypophysectomized at 60 days of age. After a post-operative control period of 15 days growth hormone (NIH-GH-B16) was given daily for 5 or 10 days followed by a 10 day period after its withdrawal. L-thyroxine was given in association with the growth hormone administration to potentiate the growth stimulation. A linear log dose-response relation was found for the two administration models with a high precision. The thyroxine-treatment increased the sensitivity of the bioassay. An administration period of 5 days was found sufficient for the bioassay of growth hormone in thyroxine-treated hypophysectomized rats. Compared with the earlier bioassay methods for growth hormone, the present bioassay is more favourable when all the factors, such as precision, sensitivity, specificity, and administration period are considered.


Author(s):  
MANOBHARATHI VENGAIMARAN ◽  
KALAIYARASI DHAMODHARAN ◽  
MIRUNALINI SANKARAN

Objective: The central motive of this study is to explore the therapeutic impact of Diosgenin encapsulated Chitosan nanoparticles (DG@CS-NP) on mammary carcinogenesis in female Sprague Dawley rats via modulating hormonal status, cell proliferation, inflammatory responses, and Apoptosis. Methods: 7,12-dimethylbenz(a)anthracene (DMBA) was administered subcutaneously near the mammary gland (25 mg/kg b. wt) to provoke mammary tumor in female Sprague Dawley rats. Following the progress of a tumor, DMBA-induced tumor-bearing rats were medicated orally with 5 mg/kg b. wt of DG@CS-NP. Consequently, the expression of ER, PR, PCNA, Cyclin D1, NF-κB, TNF-α, Bcl-2, Caspases-3, and p53 in experimental rats were revealed via architectural immunohistochemistry. Further, Diosgenin interactions with these proteins were evidently confirmed by molecular docking analysis. Results: As a result, we noticed diminished levels of ER, PR, PCNA, Cyclin D1, NF-κB, TNF-α, and Bcl-2 expressions in DG@CS-NP medicated rats as well as with elevated levels of Caspases-3 and p53 expressions. In DMBA rats, the expressions were vice versa. Additionally, molecular docking analyses support these outcomes by highlighting the strong interaction between Diosgenin and breast cancer targets. Conclusion: These reports prove that DG@CS-NP imposes its therapeutic impact by hormonal adjustments, downregulating proteins involved in inflammation and cellular proliferation, and thereby promotes apoptosis by impeding apoptotic inhibitors.


1991 ◽  
Vol 74 (3) ◽  
pp. 487-491 ◽  
Author(s):  
Christer Dahlin ◽  
Per Alberius ◽  
Anders Linde

✓ Various techniques for treatment of large cranial defects have been reported, but the use of alloplastic materials still seems to predominate. The authors have applied and explored a new approach for bone repair which appears promising, even for use in less osteogenic environments such as the adult calvaria. Seventy-two adult Sprague-Dawley rats each received bilateral 8-mm trephine defects in the temporoparietal area; this defect size precludes spontaneous osseous healing during the lifetime of the animal. Five surgical procedures, employing various alternatives of biologically inert expanded polytetrafluoroethylene membrane positioning and intramembranous bone-chip implantation, were performed and compared to control defects. Slight improvement of bone regeneration was demonstrated with subperiosteal ectocranial and endocranial membranes, alone or in combination, and with bone chips alone or in combination with an outer or inner membrane. Virtually complete bone healing was observed in animals receiving both an outer and an inner membrane with interpositioned bone chips. The latter appeared to function primarily as space-holders by keeping the membranes separated throughout the defect. Consequently, this technique seems to significantly promote bone repair by excluding soft-tissue components from the bone-healing site.


2012 ◽  
Vol 302 (1) ◽  
pp. G145-G152 ◽  
Author(s):  
Vairappan Balasubramaniyan ◽  
Gavin Wright ◽  
Vikram Sharma ◽  
Nathan A. Davies ◽  
Yalda Sharifi ◽  
...  

Ammonia is central in the pathogenesis of hepatic encephalopathy, which is associated with dysfunction of the nitric oxide (NO) signaling pathway. Ornithine phenylacetate (OP) reduces hyperammonemia and brain water in cirrhotic animals. This study aimed to determine whether endothelial NO synthase activity is altered in the brain of cirrhotic animals, whether this is associated with changes in the endogenous inhibitor, asymmetric-dimethylarginine (ADMA) and its regulating enzyme, dimethylarginine-dimethylaminohydrolase (DDAH-1), and whether these abnormalities are restored by ammonia reduction using OP. Sprague-Dawley rats were studied 4-wk after bile duct ligation (BDL) ( n = 16) or sham operation ( n = 8) and treated with placebo or OP (0.6 g/kg). Arterial ammonia, brain water, TNF-α, plasma, and brain ADMA were measured using standard techniques. NOS activity was measured radiometrically, and protein expression for NOS enzymes, ADMA, DDAH-1, 4-hydroxynonenol (4HNE), and NADPH oxidase (NOX)-1 were measured by Western blotting. BDL significantly increased arterial ammonia ( P < 0.0001), brain water ( P < 0.05), and brain TNF-α ( P < 0.01). These were reduced significantly by OP treatment. The estimated eNOS component of constitutive NOS activity was significantly lower ( P < 0.05) in BDL rat, and this was significantly attenuated in OP-treated animals. Brain ADMA levels were significantly higher and brain DDAH-1 significantly lower in BDL compared with sham ( P < 0.01) and restored toward normal following treatment with OP. Brain 4HNE and NOX-1 protein expression were significantly increased in BDL rat brain, which were significantly decreased following OP administration. We show a marked abnormality of NO regulation in cirrhotic rat brains, which can be restored by reduction in ammonia concentration using OP.


2017 ◽  
Vol 1 (S1) ◽  
pp. 60-60
Author(s):  
Andrea Lee Frump ◽  
Margie Albrecht ◽  
Sandra Breuils-Bonnet ◽  
Bakhtiyor Yakubov ◽  
Mary Beth Brown ◽  
...  

OBJECTIVES/SPECIFIC AIMS: Women with pulmonary arterial hypertension (PAH) exhibit superior right ventricular (RV) function and survival compared with men, a phenomenon attributed to poorly understood cardioprotective effects of 17β-estradiol (E2). We hypothesize that E2, through ERα, attenuates PH-induced RV dysfunction by upregulating the pro-contractile and pro-angiogenic peptide apelin. This ERα-mediated increase in apelin is mediated by the myocardial remodeling effector bone morphogenetic protein receptor 2 (BMPR2). METHODS/STUDY POPULATION: ERα, BMPR2, and apelin were measured (western blot) in RVs from patients with PAH-induced RV failure and in RV homogenates from male or female Sprague-Dawley rats with sugen/hypoxia (SuHx) or monocrotaline (MCT)-induced PH. H9c2 rat cardiomyoblasts and cardiac endothelial cells were stressed with TNF-α (10 ng/mL) or staurosporine (50 nM)±E2 (100 nM; 24 h). ERα-, BMPR2-, and apelin-dependence were evaluated by siRNA (5 pM). Downstream apelin target and pro-survival factor ERK1/2 expression was measured (western blot). p<0.05 by ANOVA was considered significant. RESULTS/ANTICIPATED RESULTS: ERα correlated positively with BMPR2 and apelin expression in SuHx-RVs and human RVs. Treatment of SuHx-PH rats with E2 or ERα agonist increased RV BMPR2 and apelin, whereas RV apelin was decreased in E2-treated hypoxic ERα knockout mice (p<0.05), but not in ERβ knockout mice. In H9c2 cells, E2 or ERα agonist attenuated TNF-α- or staurosporine-induced decreases in BMPR2, apelin, and phospho-ERK1/2 (p<0.05 for all endpoints). E2 protection was lost in presence of siRNA directed against ERα, BMPR2, or apelin (p<0.05). ERα was necessary for E2-mediated increases in BMPR2, apelin, and ERK1/2, and BMPR2 was required for the E2-mediated increase in apelin (p<0.05 for siRNA vs. scramble). ERα, BMPR2, and apelin protein was increased in decompensated human RVs but downstream phospho-ERK signaling was disrupted. DISCUSSION/SIGNIFICANCE OF IMPACT: E2, via ERα, increases BMPR2 and apelin in the failing RV and in stressed rat cardiomyoblasts. The E2-mediated increase in apelin is BMPR2-dependent and likely occurs through direct binding of ERα to the BMPR2 promoter. Harnessing this E2-ERα-BMPR2-apelin axis during RV compensation may lead to novel, RV-targeted therapies for PAH patients of either sex.


2003 ◽  
Vol 284 (4) ◽  
pp. R916-R927 ◽  
Author(s):  
Zhi-Hua Zhang ◽  
Shun-Guang Wei ◽  
Joseph Francis ◽  
Robert B. Felder

In pathophysiological conditions, increased blood-borne TNF-α induces a broad range of biological effects, including activation of the hypothalamic-pituitary-adrenal axis and sympathetic drive. In urethane-anesthetized adult Sprague-Dawley rats, we examined the mechanisms by which blood-borne TNF-α activates neurons in paraventricular nucleus (PVN) of hypothalamus and rostral ventrolateral medulla (RVLM), two critical brain regions regulating sympathetic drive in normal and pathophysiological conditions. TNF-α (0.5 μg/kg), administered intravenously or into ipsilateral carotid artery (ICA), activated PVN and RLVM neurons and increased sympathetic nerve activity, arterial pressure, and heart rate. Responses to intravenous TNF-α were not affected by vagotomy but were reduced by mid-collicular decerebration. Responses to ICA TNF-α were substantially reduced by injection of the cyclooxygenase inhibitor ketorolac (150 μg) into lateral ventricle. Injection of PGE2 (50 ng) into lateral ventricle or directly into PVN increased PVN or RVLM activity, respectively, and sympathetic drive, with shorter onset latency than blood-borne TNF-α. These findings suggest that blood-borne cytokines stimulate cardiovascular and renal sympathetic responses via a prostaglandin-dependent mechanism operating at the hypothalamic level.


Pharmacology ◽  
2019 ◽  
Vol 104 (1-2) ◽  
pp. 71-80 ◽  
Author(s):  
Ying Zhang ◽  
Shaoyu Ren ◽  
Ying Ji ◽  
Yafeng Liang

Background: Our study investigated the therapeutic role and potential mechanisms of pterostilbene (PS) in diabetic nephropathy (DN) rats. Methods: DN models were established by high-fat diet after streptozotocin injection. A total of 50 Sprague-Dawley rats were randomly divided into control, DN, PS-treated groups (PS-H, PS-M, PS-L). PS was administered to rats by gavage for 8 weeks at 3 different doses (25, 10, and 5 mg/kg/day). The levels of oxidative stress activity (superoxide dismutase [SOD], malondialdehyde [MDA], glutathione peroxidase [GSH-PX]) and inflammatory factors (tumor necrosis factor [TNF]-α, interleukin (IL)-6, IL-1β, monocyte chemoattractant factor [MCP]-1) were detected by ­ELISA. TGF-β, Smad1, and fibronectin (FN) were measured through immunohistochemistry. The relative expressions of phospho-IκBα/IκBα, phospho-IκB kinases (IKK)β/IKKβ, phospho-nuclear factor-κB (NF-κB) p65/NF-κB p65 were detected by western blot. Results: Compared with DN group, the levels of TNF-α, IL-6, IL-1β, and MCP-1 were decreased in the PS-H group (p < 0.05). Meanwhile, the levels of SOD, MDA, GSH-PX improved in kidney and serum in PS-H groups (p< 0.05). PS also significantly decreased the level of phospho-NF-κB p65 and increased the levels of phospho- IKKβ and phospho-Iκ-Bα (p < 0.05). The results showed that PS treatment decreased TGF-β, Smad1, and FN expressions. Conclusion: PS had potential therapeutic effects on DN, which may be related to the regulation of NF-κB pathway.


2010 ◽  
Vol 108 (6) ◽  
pp. 1737-1744 ◽  
Author(s):  
Olli V. Leppänen ◽  
Harri Sievänen ◽  
Jarkko Jokihaara ◽  
Ilari Pajamäki ◽  
Pekka Kannus ◽  
...  

This study evaluated the contributions of locomotive loading and estrogen to the development of diaphysis of rat femur. A randomized 2 × 2 study design was used. Altogether, 70 female Sprague-Dawley rats were used, of which 10 were euthanized at entry. Of the remaining rats, 16 served as controls, and the rest, 44, underwent a unilateral sciatic neurectomy. The effect of estrogen was removed by ovariectomizing one-half of the neurectomized rats. After 27 wk, the animals were euthanized, and the femora were excised. Irrespective of loading or estrogen, the femur length and mineral mass increased by 142 and 687%, respectively. Axial growth was not modulated either by locomotive loading or estrogen, but the loading resulted in direction-specific changes in the cross-sectional geometry. The estrogen-related gains were evident on the endocortical surface, while the loading-related gains occurred on the periosteal surface. The loading and estrogen were significantly associated with increased bone strength (21 and 15%, respectively) in the mediolateral direction, but not in the anteroposterior direction. Axial growth and accrual of bone mineral mass of the rat femur are largely independent of locomotive loading or estrogen, whereas these factors specifically account for the femur function, as either a mechanical lever or a mineral reservoir for reproduction, respectively.


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