Objective: The purpose of this study was to compare the effects of the selective serotonin reuptake inhibitor (SSRI) fluoxetine and the serotonin-norepinephrine reuptake inhibitor (SNRI) venlafaxine on bone defect healing.
Materials And Methods: Wistar rats were randomly divided into three groups of eight animals each. The first received 0.1 ml/kg sterile saline solution, the second 5 mg/kg fluoxetine, and the third 5 mg/kg venlafaxine, daily by gastric gavage over 7 weeks. At week 3 of drug therapy, 5-mm diameter calvarial defects were created in the parietal bone of all of the animals. All rats were euthanized four weeks after surgery, micro-CT analysis and histomorphometric analysis were carried out to evaluate the following parameters: Bone volume fraction (BV/TV), bone surface (BS), bone surface density (BS/BV; bone surface/bone volume, 1/mm), trabecular number (Tb. N), trabecular thickness (Tb. Th), areas of new bone structure (positive areas), areas of mature bone structure (negative areas).
Results: Micro-CT analysis showed the presence of similar levels of bone formation within the defect site in all three groups (p>0.05). Histomorphometric analysis revealed the presence of bone-forming cells at the defect periphery, with less activity indicating bone formation at the center. No statistically significant difference was observed between the groups (p>0.05).
Conclusion: Based on the findings of this study, it can be said that the use of both antidepressants hasn't any effect on bone defect healing.
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http://dx.doi.org/10.1016/j.injury.2023.03.034 | DOI Listing |
J Clin Invest
January 2025
Department of Laboratory Medicine, Division of Translational Cancer Researc, Lund University Cancer Centre, Lund University, Lund, Sweden.
The biology centered around the TGF-beta type I receptor Activin Receptor-Like Kinase (ALK)1 (encoded by ACVRL1) has been almost exclusively based on its reported endothelial expression pattern since its first functional characterization more than two decades ago. Here, in efforts to better define the therapeutic context in which to use ALK1 inhibitors, we uncover a population of tumor-associated macrophages (TAMs) that, by virtue of their unanticipated Acvrl1 expression, are effector targets for adjuvant anti-angiogenic immunotherapy in mouse models of metastatic breast cancer. The combinatorial benefit depended on ALK1-mediated modulation of the differentiation potential of bone marrow-derived granulocyte-macrophage progenitors, the release of CD14+ monocytes into circulation, and their eventual extravasation.
View Article and Find Full Text PDFKlin Mikrobiol Infekc Lek
September 2023
Infectious Disease Department, Ceske Budejovice Hospital, Czech Repubic, e-mail:
Corynebacteria, non-spore-forming, gram-positive, aerobic or facultative anaerobic, pleomorphic bacilli, are part of the normal skin, oropharyngeal, and intestinal flora in humans. However, this microorganism can rarely be associated with invasive infections such as bone and joint infections, bacteremia, endocarditis, meningitis, liver and spleen abscesses. We present a case of bacteremic arthritis of a native knee joint caused by non-toxigenic Corynebacterium diphtheriae in a patient with alcoholic liver cirrhosis.
View Article and Find Full Text PDFImportance: Fragility fractures result in significant morbidity.
Objective: To review evidence on osteoporosis screening to inform the US Preventive Services Task Force.
Data Sources: PubMed, Embase, Cochrane Library, and trial registries through January 9, 2024; references, experts, and literature surveillance through July 31, 2024.
JAMA Netw Open
January 2025
University of Washington, Seattle.
Curr Osteoporos Rep
January 2025
Department of Immunology, Tufts University, Boston, MA, 02111, USA.
Purpose Of Review: The purpose of this review is to summarize the current understanding of cell-autonomous innate immune pathways that contribute to bone homeostasis and disease.
Recent Findings: Germ-line encoded pattern recognition receptors (PRRs) are the first line of defense against danger and infections. In the bone microenvironment, PRRs and downstream signaling pathways, that mount immune defense, interface intimately with the core cellular processes in bone cells to alter bone formation and resorption.
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