Biology subjects

Mermet, M.

Publications and source records attributed to Mermet, M..

3 recordsLinked to original sources

bioRxiv2025

Hypertrophic bone proliferation at enthesis induced by unilateral injection of botulinum toxin in masticatory muscles in adult rats is characterized by chondrocyte proliferation without inflammatory process at enthesis

A single injection of botulinum toxin injected in masticatory muscles induces alveolar bone loss associated with muscle enthesis hypertrophic bone proliferation. The tissular and cellular mechanisms involved in this phenomenon are unknown. Because new bone formation due to inflammation at enthesis is observed in articular disorder like spondyloarthritis, we hypothesize that an inflammatory process could explain the development of hypertrophic bone proliferation in the BTX model. The aims of the study were to test this hypothesis and to determine whether IL-17A was involved. Mature Sprague-Dawley male rats (n=36) were randomized into 4 groups. Three groups received BTX injections in right masseter and temporalis muscle. One BTX group was treated with an anti-IL17A antibody for 31 days (BTX31+antiIL17A). The two other groups were respectively sacrificed at 21 (BTX21) and 31 (BTX31) days post BTX injection. The remaining non-BTX group received anti-IL17A treatment for 31 days (control+anti-IL-17A). Alveolar bone loss and hypertrophic bone proliferation at enthesis were studied using microcomputed tomography. The presence of inflammatory process and the implication of IL17A was assessed by histology and immunohistochemistry on decalcified right side hemimandibles. Quantitative measurement of the hypertrophic bone (bone volume and thickness) showed no significant differences between the 3 BTX groups. Histology revealed the presence of chondrocytes in large hypertrophic area but no inflammatory infiltrated cells. Immunochemistry confirmed the absence of inflammatory process but positive reaction for Ki67 which is in favor of actively growing and proliferative chondrocytes. BTX-related muscle atrophy of masticatory muscle induced chondrocyte proliferation at enthesis without inflammation process.

pathology↗

bioRxiv2024

The GLP-1 analogue, exendin-4, improves bone material properties and strength through a central relay in ovariectomized mice

Glucagon-like peptide-1 (GLP-1) has previously been shown to be indispensable for optimal bone strength by acting at the bone material level. However, it was not fully clear whether the effects of GLP-1 were mediated by direct or indirect actions on bone cells. In the present study, we were unable to demonstrate the expression of the GLP-1 receptor (GLP-1r) in bone tissue at the gene expression level using qPCR and in situ hybridization, or at the protein level. Furthermore, the peripheral administration of exendin-4, a specific GLP-1r agonist, in ovariectomized (OVX) BALB/c mice enhanced post-yield displacement (18%) and energy-to-fracture (24%), as well as bone volume/total volume (BV/TV) (11%), trabecular number (Tb.N) (6%), and collagen maturity (18%). These bone effects were still observed when exendin-4 was centrally administered into the lateral cerebral ventricle. On the other hand, the peripheral administration of exendin-4 coupled to bovine serum albumin, a GLP-1r agonist that cannot penetrate the brain, failed to replicate the positive effects on bone despite increased calcitonin secretion. Altogether, these data confirm that GLP-1r agonists represent an interesting approach for managing bone fragility due to ovariectomy, but also suggest that GLP-1r agonists require a central relay yet to be identified to exert positive effects on bone physiology. Further studies are needed to decipher the mechanisms of action of GLP-1 and GLP-1r agonists on bone physiology.

physiology↗

bioRxiv2024

Effects of vertical sleeve gastrectomy prior to pregnancy on bone mass, microarchitecture and material properties in the female rat

Obesity is a major public health issue worldwide. Despite various approaches to weight loss, the most effective technique for reducing obesity, as well as diabetes and associated diseases, is bariatric surgery. Increasingly, young women without children are undergoing bariatric surgery, vertical sleeve gastrectomy (VSG) being the most common procedure nowadays. However, despite several reports suggesting bone loss after VSG, little is known about the potential additive effects of gestation and lactation after VSG to bone health. This study investigated the combined effects of pre-gestational VSG and subsequent gestation/lactation on bone metabolism in a rat model fed a high fat high sugar (HFHS) diet, with a focus on bone biomechanics, mass, microarchitecture and material properties. Furthermore, bone mass and remodelling was followed longitudinally by microCT prior to surgery, 4 weeks post-surgery, after weaning and at sacrifice. Significant alterations in bone mass and microarchitecture, characterized by changes in trabecular thickness and number, as well as changes in bone formation and resorption were influenced by both surgery and reproductive demands. Mechanical testing at sacrifice demonstrated compromised long bone fragility, in rat with HFHS regardless of the surgical procedure (Sham or VSG). Furthermore, analysis of bone material properties highlighted potential disruptions in the pattern of bone mineralization in sham and VSG animals fed a HFHS diet. These findings underscore the complex interplay between pre-gestational VSG and subsequent gestation/lactation in modulating bone metabolism. Understanding these combined effects is essential for optimizing surgical strategies and developing targeted interventions to mitigate potential bone-related complications associated with VSG in reproductive-aged individuals.

physiology↗