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Patients with spinal cord injury (SCI) undergo severe loss of bone mineral below the level of lesion, and data on available treatment options after SCI is scarce. The aim of this work was to investigate the therapeutic effect of cannabidiol (CBD), a non-psychoactive cannabis, on sublesional bone loss in a rat model of SCI. The adult male rats were exposed to surgical transection of the cord and treated with CBD for consecutive 14 days. It was found that CBD treatment elevated the serum levels of osteocalcin, reduced the serum levels of collagen type I cross-linked C-telopeptide, and enhanced bone mineral density of tibiae and femurs. Treatment of SCI rats with CBD enhanced bone volume, trabecular thickness, and trabecular number, and reduced trabecular separation in proximal tibiae, and increased ultimate compressive load, stiffness, and energy to max force of femoral diaphysis. Treatment of SCI rats with CBD upregulated mRNA expression of alkaline phosphatase and osteoprotegerin and downregulated mRNA expression of receptor activator of NF-κB ligand and tartrate-resistant acid phosphatase in femurs. Furthermore, treatment of SCI rats with CBD enhanced mRNA expression of wnt3a, Lrp5 and ctnnb1 in femurs. In conclusion, CBD administration attenuated SCI-induced sublesional cancellous bone loss.
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http://dx.doi.org/10.1016/j.ejphar.2017.05.011 | DOI Listing |
Arterioscler Thromb Vasc Biol
September 2025
Department of Medicine/Division of Cardiology, University of California Los Angeles. (S.S., C.R.S., L.F., M.P., C.P., Z.Z., J.J.M., R.C.D., D.S., A.J.L.).
Background: In genetic studies with the Hybrid Mouse Diversity Panel, we previously identified a chromosome 9 locus for atherosclerosis. We now identify NNMT (nicotinamide -methyltransferase), an enzyme that degrades nicotinamide, as the causal gene in the locus and show that the underlying mechanism involves salvage of nicotinamide to nicotinamide adenine dinucleotide (NAD).
Methods: Gain/loss of function studies in macrophages were performed to examine the role of NAD levels in macrophage proliferation and apoptosis in atherosclerosis.
Periodontol 2000
September 2025
Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, Michigan, USA.
This systematic review and meta-analysis aimed to evaluate the long-term clinical outcomes of regenerative procedures compared with access flap surgery for the treatment of intrabony defects, with a minimum follow-up period of 5 years. A systematic review protocol following PRISMA guidelines was conducted. Both electronic and manual searches were conducted to identify randomized clinical trials (RCTs) on regenerative treatment of deep intrabony defects (≥3 mm) with a follow-up of at least 5 years.
View Article and Find Full Text PDFJ Orthop Res
September 2025
Institute of Orthopaedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Osteoporotic hip fractures are a considerable cause of pain and disability particularly among the elderly. Osteoporosis causes loss of bone stability, which in turn leads to an increased risk of fractures especially in metaphyseal bone. Moreover, the body's capacity for healing is diminished, resulting in prolonged recovery times following these fractures.
View Article and Find Full Text PDFClin Oral Investig
September 2025
Department of Stomatology, Shengli Oilfield Central Hospital, No. 31, Jinan Road, Dongying, 257034, China.
Objective: Progesterone (PG) and its target, progesterone receptor (PGR), are important regulators in inflammatory diseases. This study aimed to investigate the specific role of PG in periodontitis and to elucidate the underlying mechanisms involving PGR.
Methods: Women with periodontitis, including 250 with PG deficiency, 250 with PG supplementation, and 245 controls (normal PG) were enrolled.
BMJ Case Rep
September 2025
Department of Pathology and Lab Medicine, All India Institute of Medical Sciences Jodhpur, Jodhpur, Rajasthan, India.
Gaucher's disease (GD) is the most common lysosomal storage disorder inherited in an autosomal recessive pattern. It occurs due to a deficiency of the enzyme glucocerebrosidase owing to a mutation in the acid-β-glucosidase () gene resulting in accumulation of glucocerebrosides in lysosomes of cells. It presents with abdominal distension, hepatosplenomegaly, developmental delay, pancytopenia, neurological manifestations and bone diseases.
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