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Fibrous Dysplasia (FD) is a benign and rare genetic disease characterized by progressive replacement of normal bone by a non-mineralized matrix. FD is caused by GNAS mutations that increase intracellular cAMP levels. While appendicular lesions have been extensively studied to enhance understanding and management of the disease, the pathogenesis of craniofacial lesions remains poorly described despite the embryological, phenotypic and mechanical differences between these two skeletal regions. Our objective was to evaluate the impact of craniofacial FD on bone homeostasis. Typical histological features, suh as “alphabet soup” appearance, were observed in craniofacial FD lesions. Higher intracellular cAMP levels were also noted in FD cultures derived from craniofacial lesions. We demonstrated an increased proliferative capacity in craniofacial FD osteoblasts, associated with decreased osteoblastic differentiation and a lack in mineralization abilities. Interestingly, we highlighted a decreased osteoclastogenic potential due to impaired osteoclast formation in FD-conditioned medium cultures, indicating a diminished osteoclastogenic potential of craniofacial FD osteoblasts. Our data suggest shared characteristics between osteoblasts from the craniofacial and the appendicular skeletons but also discrepancies regarding osteoclastic potential. Exploring these features could help explain the differences observed between appendicular and cranio-facial lesions and should lead to further studies on the pathogenesis of craniofacial fibrous dysplasia.

is a commensal skin bacterium that is involved in bone prosthesis infections (BPIs) and presents low-grade clinical symptoms. has been thought to escape the immune system at bone sites. Our study was carried out on a laboratory strain and two BPI-related clinical strains, one of which surprisingly induced clinical symptoms of inflammation in the patient. We investigated the ability of these strains to trigger human primary neutrophils (PMN) response through inflammatory mediators measurements (antibody arrays, ELISA, RT-qPCR, zymography) and activation status assessment (flow cytometry), and to induce PMN recruitment from the bloodstream in mice air-pouch model. PMN-mediated inflammation was also studied in an original model mimetic of an infected bone site that combine titanium alloy, human primary osteoblasts, human primary neutrophils and strains. We demonstrated for the first time that both planktonic and biofilm cultures, triggered an effective immune response by neutrophils and their recruitment . This host response was enhanced when using a strain from a patient with inflammatory signs. In an original infected prosthesis mimetic model, osteoblasts and neutrophils were able to detect , but their response to the clinical inflammatory strain decreased. This work provides the first evidence showing that the immune cell response to pathogenic may be tuned by nonimmune cells at the infected site, such as osteoblasts, which may promote bacterial persistence.

Cariogenic Streptococcus mutans ( S. mutans ) is implicated in the dental pulp necrosis but also in cardiovascular tissue infections. Herein, the purpose was to elucidate how human dental pulp derived stromal cells (DPSCs) react toward a direct interaction with S. mutans . DPSCs were challenged with S. mutans . Following 3 h of interaction, DPSCs were able to internalize S. mutans (rate < 1%), and F-actin fibers played a significant role in this process. S. mutans persisted in the DPSCs for 48 h without causing a cytotoxic effect. S. mutans was, however, able to get out of the DPSCs cytoplasm and to proliferate in the extracellular environment. Yet, we noticed several adaptive responses of bacteria to the extracellular environment such as a modification of the kinetic growth, the increase in biofilm formation on type I collagen and polyester fabrics, as well as a tolerance toward amoxicillin. In response to infection, DPSCs adopted a proinflammatory profile by increasing the secretion of IL-8, lL-1β, and TNF-α, strengthening the establishment of the dental pulp inflammation. Overall, these findings showed a direct impact of S. mutans on DPSCs, providing new insights into the potential role of S. mutans in infective diseases.

Schwannomas are benign peripheral nerve sheath tumors originating from the Schwann cells. Most schwannomas in the head and neck region are solitary; however, multiple schwannomas affecting one or more nerves suggest a possible association with neurofibromatosis type 2 and schwannomatosis. Plexiform schwannoma is a rare variant of conventional schwannoma that is characterized by intraneural multinodular growth. This grow pattern has also been observed with other neural tumors which may make diagnosis more difficult. Herein, we report the case of a 28-year-old woman who presented a solitary plexiform schwannoma of great palatine nerve. In the present case, we focused on immunohistochemical analysis in daily practice for the differential diagnosis of schwannomas and their mainly morphological mimics, especially with plexiform neurofibroma, granular cell tumor and malignant peripheral nerve sheath tumors. We also discussed on SMARBC1/IN1 marker usefulness in combination with brain magnetic resonance imaging for the distinction of solitary schwannoma from neurofibromatosis type 2 or schwannomatosis.

While stem cell/biomaterial studies provide solid evidences that biomaterial intrinsic cues deeply affect cell fate, current strategies tend to neglect their effects on mesenchymal stem cells (MSCs) secretory activities and resulting cell-crosstalks. The present study aims to investigate the impact of bone-mimetic material (B-MM), with intrinsic osteoinductive property, on MSCs mediator secretions; and to explore underlying effects on cells involved in bone regeneration. Human MSCs were cultured, on B-MM, made from inorganic calcium phosphate supplemented with chitosan and hyaluronic acid biopolymers. Collected MSCs culture media were assessed for mediators release quantification and used further to stimulate endothelial cells (ECs) and alveolar bone derived osteoblasts (OBs). Without osteogenic supplements, MSCs committed into bone lineage forming thus 3D bone- like nodules after 21 days. Despite a weak percentage of cell commitment, our data elucidate new aspects of osteoinductive material effect on MSCs functions through the regulation of the secretion of mediators involved in bone regeneration and subsequently the MSCs/ECs indirect crosstalk with osteogenesis-boosting effect. Using MSCs culture media, we demonstrate a large potential of osteoinductive materials and MSCs in bone regenerative medicine. Such strategies could help to address some insights in cell-free therapies using MSCs derived media.

Introduction: Cystinosis is a rare genetic disease due to a defective transport of cystine out of the lysosomes, caused by a mutation of the gene encoding for the lysosomal carrier protein, the cystinosin. Cystine accumulation results in the formation of intracellular cystine cristals, that causes tissular and multi-organic lesions (kidney, eyes, endocrine glands). Observation: We report a rare case of a patient affected by infantile nephropathic cystinosis, who consulted for an implant placement in a single-tooth gap. Discussion: Accumulation of cystine leads to tissue damage, primarily in the kidney, the liver and the cornea, but other organs, such as the mouth, teeth and jaws may be also involved. The article aimed to present oral manifestations associated with this storage disease and to discuss how oral surgeon can evaluate and manage these patients despite the lack of a standardized protocol.

Background: The induced membrane (IM) preclinical models have been described in small animals, but few studies have looked at bone regeneration achievement. The optimisation and validation of such a preclinical model, considering the results obtained after the use of biomaterials as a substitute for bone grafting, could lead to simplifying the surgical procedure and enhance the clinical results. Methods: An in vivo model of the IM technique was developed on the femur of Lewis rats after a 4‐mm critical bone defect stabilised with an osteosynthesis plate. A first optimisation phase was performed by evaluating different osteotomy methods and two different osteosynthesis plate sizes. The efficiency of the model was evaluated by the failure rate obtained 6 weeks after the first operative time. Thereafter, bone regeneration was evaluated histologically and radiologically at 24 weeks to confirm the critical nature of the bone defect (negative control), the effectiveness of the IM with a syngeneic bone graft (positive control) and the possibility of using a biomaterial (GlassBone Noraker) in this model. Results: Sixty‐three rats were included and underwent the first surgical step. Nineteen rats subsequently underwent the second surgical step. The results obtained led to select piezotomy as the best osteotomy technique and 1‐mm‐thick plates with 2.0‐mm‐diameter screws as osteosynthesis material. Twenty‐four weeks after the second surgical step, solely the group with both surgical steps and a syngeneic bone graft showed complete ossification of the bone defect. In contrast, the group without a graft did not present a suitable ossification, which confirms the critical nature of the defect. IM produced an incomplete bone regeneration using GlassBone alone. Conclusions: A piezotome osteotomy with an osteosynthesis plate of sufficient stiffness is required for this two‐stage bone regeneration model in rats. The 4‐mm bone defect is critical for this model and suitable for biomaterial evaluation.