Bone最新文献

{"title":"High-resolution microCT analysis of sclerotic subchondral bone beneath bone-on-bone wear grooves in severe osteoarthritis","authors":"Meret Keiser ,&nbsp;Stefan Preiss ,&nbsp;Stephen J. Ferguson ,&nbsp;Vincent A. Stadelmann","doi":"10.1016/j.bone.2024.117388","DOIUrl":"10.1016/j.bone.2024.117388","url":null,"abstract":"<div><div>Osteoarthritis (OA) is associated with sclerosis, a thickening of the subchondral bone plate, yet little is known about bone adaptations around full-thickness cartilage defects in severe knee OA, particularly beneath bone-on-bone wear grooves. This high-resolution micro-computed tomography (microCT) study aimed to quantify subchondral bone microstructure relative to cartilage defect location, distance from the joint space, and groove depth.</div><div>Ten tibial plateaus with full-thickness cartilage defects were microCT-scanned to determine defect location and size. Wear groove depth was estimated as the thickness from its deepest point to a surface interpolated from the defect edges. Two 5 × 5 mm specimens were sampled from three regions (defect, edge, and cartilage-covered areas) and two from the contralateral condyle, then scanned at higher resolution. Bone density profiles were analyzed as a function of distance from the joint space to identify cortical and trabecular regions of interest and and compute their respective bone density and microstructure.</div><div>Cortical bone beneath defects was four times thicker under wear grooves than beneath cartilage. Bone density profiles significantly differed between the three specimen types at depths up to 5 mm. Below defects, cortical porosity was 85 % higher, and trabecular density 14 % higher, than in cartilage-covered specimens. Some trabecular spaces were filled with woven bone-like tissue, forming a new cortical layer. These changes were confined to the defect region and ceased abruptly at the defect edge. No correlation was found between bone microstructural indices and the estimated groove depth.</div><div>Our findings suggest an ongoing migration of the cortical layer during formation of the groove from its original position into the underlying trabecular bone, a process we termed “trabecular corticalization.” Under deeper wear grooves, the new cortical layer exhibited large pores connecting bone marrow to the joint space, suggesting physiological limits to corticalization. These results highlight specific bone adaptations beneath cartilage defects in severe OA and provide insights into the progression of subchondral bone changes under bone-on-bone contact areas.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"193 ","pages":"Article 117388"},"PeriodicalIF":3.5,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142973892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiscale interstitial fluid computation modeling of cortical bone to characterize the hydromechanical stimulation of lacunar-canalicular network","authors":"WeiLun Yu ,&nbsp;RenXia Ou ,&nbsp;Qi Hou ,&nbsp;ChunMing Li ,&nbsp;XiaoHang Yang ,&nbsp;YingHui Ma ,&nbsp;XiaoGang Wu ,&nbsp;WeiYi Chen","doi":"10.1016/j.bone.2024.117386","DOIUrl":"10.1016/j.bone.2024.117386","url":null,"abstract":"<div><div>Bone tissue is a biological composite material with a complex hierarchical structure that could continuously adjust its internal structure to adapt to the alterations in the external load environment. The fluid flow within bone is the main route of osteocyte metabolism, and the pore pressure as well as the fluid shear stress generated by it are important mechanical stimuli perceived by osteocytes. Owing to the irregular multiscale structure of bone tissue, the fluid stimulation that lacunar-canalicular network (LCN) in different regions of the tissue underwent remained unclear. In this study, we constructed a multiscale conduction model of fluid flow stimulus signals in bone tissue based on the poroelasticity theory. We analyzed the fluid flow behaviors at the macro-scale (whole bone tissue), macro-<em>meso</em> scale (periosteum, interstitial bone, osteon and endosteum), and micro-scale (lacunar-osteocyte-canalicular) levels. We explored how fluid stimulation at the tissue level correlated with that at the cellular level in cortical bone and characterized the distributions of the pore pressure, fluid velocity and fluid shear stress that the osteocytes experienced across the entire tissue structure. The results showed that the initial conditions of intramedullary pressure had a significant impact on the pore pressure of Haversian systems, but had a relatively small influence on the fluid velocity. The osteocyte which were located at different positions in the bone tissue received very distinct fluid stimuli. Osteocytes in the vicinity of the Haversian Canals experienced higher fluid shear stress stimulation. When the permeability of the LCN was within the range from 10⁻²¹ m² to 10⁻¹⁸ m², the distribution of pressure, fluid velocity and fluid shear stress within the osteon near the periosteum and endosteum was significantly different from that in other parts of the bone. However, when the permeability was less than 10⁻²² m², such a difference did not exist. Particularly, the flow velocity at the lacunae was markedly higher than that in the canaliculi. Meanwhile, the pore pressure and fluid shear stress were conspicuously lower than those in the canaliculi. In this study, we considered the interconnections of different biofunctional units at different scales of bone tissue, construct a more complete multiscale model of bone tissue, and propose that osteocytes at different locations receive different fluid stimuli, which provides a reference for a deeper understanding of bone mechanotransduction.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"193 ","pages":"Article 117386"},"PeriodicalIF":3.5,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142924188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obesity and insulinopenic type 2 diabetes differentially impact, bone phenotype, bone marrow adipose tissue, and serum levels of the cathelicidin-related antimicrobial peptide in mice","authors":"Amélie Paquet ,&nbsp;Nadia Bahlouli ,&nbsp;Xavier Coutel ,&nbsp;Damien Leterme ,&nbsp;Jérôme Delattre ,&nbsp;Véronique Gauthier ,&nbsp;Flore Miellot ,&nbsp;Séverine Delplace ,&nbsp;Hélène Rouge-Labriet ,&nbsp;Nicolas Bertheaume ,&nbsp;Christophe Chauveau ,&nbsp;Hamanou Benachour","doi":"10.1016/j.bone.2024.117387","DOIUrl":"10.1016/j.bone.2024.117387","url":null,"abstract":"<div><div>Obesity is a risk factor of developing type 2 diabetes (T2D) and metabolic complications, through systemic inflammation and insulin resistance. It has also been associated with increased bone marrow adipocytes along with increased bone fragility and fracture risk. However, the differential effects of obesity and T2D on bone fragility remain unclear. The cathelicidin-related antimicrobial peptide (CRAMP) is a multifunctional modulator of the innate immunity that has emerged as biomarker of cardiometabolic diseases. The aims of this study were i) to assess the differential impact between hyperinsulinemic obesity versus insulinopenic T2D, on bone phenotype and bone marrow adipose tissue (BMAT), and ii) to analyse the link with CRAMP expression and its circulating levels in the context of obesity and T2D. We used C57BL/6 J male mice models of obesity induced by high-fat diet (HFD), and of insulinopenic T2D induced by streptozotocin (STZ) treatment combined with HFD, reflecting the metabolic heterogeneity of the diseases. As compared to low-fat diet (LFD) control group after 16 weeks of feeding, the HFD mice exhibit a significant weight gain, moderate hyperglycaemia, impaired glucose tolerance and insulin sensitivity, and significant increase in serum insulin levels. This hyperinsulinemic obesity led to decreased trabecular (Tb.Th) and cortical thickness (Ct.Th) in the tibia, associated with significant BMAT expansion, in addition to increased subcutaneaous (SCAT) and visceral adipose tissue (VAT). No changes were observed in the circulating levels of CRAMP peptide neither in other bone parameters. While, STZ treatment in HFD/STZ group induced a more severe hyperglycaemia, glucose intolerance and insulin resistance, and hypoinsulinemia. We also observed a negative effect on the expansion of both SCAT and VAT, as well as lower increase in BMAT as compared to HFD group. However, these mice with insulinopenic T2D exhibit early decrease in trabecular number (Tb.N) in proximal tibia, progressively from 8 to 16 weeks of protocol, and impaired femoral biomechanical stiffness. These alterations are also accompanied with decreased circulating levels of the CRAMP peptide in the HFD/STZ mice. The CRAMP mRNA levels decreased in VAT of both HFD and HFD/STZ groups.</div><div>Overall, these results provide novel insights into the differential negative impact of obesity versus T2D on bone microenvironment, and suggest a link between hyperglycaemia-induced bone quality alterations during insulinopenia, and impaired regulation of the cathelicidin peptide of the innate immunity. Further investigations are needed to elucidate this relationship.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"193 ","pages":"Article 117387"},"PeriodicalIF":3.5,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142916565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Primary components of MCT ketogenic diet are detrimental to bone loss associated with accelerated aging and age-related neurotoxicity in mice","authors":"Shreshta Jain,&nbsp;Divya Vohora","doi":"10.1016/j.bone.2024.117383","DOIUrl":"10.1016/j.bone.2024.117383","url":null,"abstract":"<div><div>Medium chained triglycerides (MCT) ketogenic diet is being extensively investigated for its neuroprotective effects against adverse effects associated with aging and neurodegenerative disorders. Aging is a common risk factor for the development of both osteoporosis and neurological disorders. Hence, suppression of aging and age-related neurodegeneration might contribute to delaying skeletal aging. The present study was designed to investigate the effects of the primary components of the MCT diet, against bone resorption associated with D-gal-induced accelerated aging and D-gal /AlCl₃-induced age-related toxicity. We report bone loss in accelerated aged mice and age-related neurotoxic mice through declined Sirtuin1 (SIRT1) expression, depleted bone turnover markers, (P1NP and β-CTX-1), low bone mineral density (BMD), and deterioration of trabecular bone microarchitecture in both the distal femur and proximal tibia bones. Administration of MCT dietary components decanoic acid and octanoic acid, led to a decrease in body weight and only octanoic acid increased serum levels of ketone body, β-hydroxybutyrate (β-HB), but both of them failed to reverse the diminishing effects on bone health associated with aging and age-related neurotoxicity. Surprisingly, decanoic acid, octanoic acid, and their combination also exhibited negative effects on trabecular bone microarchitecture and BMD in the distal femur and proximal tibia bones of healthy mice. The findings from this study provide supporting evidence on the deterioration of bone health associated with aging and age-related neurotoxicity, and the bone resorption potential of MCT dietary supplements that are being prescribed in healthy older populations and elderly persons diagnosed with neurological disorders.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"192 ","pages":"Article 117383"},"PeriodicalIF":3.5,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PTX3-assembled pericellular hyaluronan matrix enhances endochondral ossification during fracture healing and heterotopic ossification","authors":"Wei Dong,&nbsp;Chang Yang,&nbsp;Donghua Guo,&nbsp;Meie Jia,&nbsp;Yan Wang,&nbsp;Jiawei Wang","doi":"10.1016/j.bone.2024.117385","DOIUrl":"10.1016/j.bone.2024.117385","url":null,"abstract":"<div><div>Endochondral ossification (EO) is a pivotal process during fracture healing and traumatic heterotopic ossification (HO), involving the cartilaginous matrix synthesis and mineralization. Unlike the extracellular matrix, the hyaluronan (HA)-rich pericellular matrix (PCM) directly envelops chondrocytes, serving as the frontline for extracellular signal reception and undergoing dynamic remodeling. Pentraxin 3 (PTX3), a secreted glycoprotein, facilitates HA matrix assembly and remodeling. However, it remains unclear whether PTX3 affects EO by regulating HA-rich PCM assembly of chondrocytes, thereby impacting fracture healing and traumatic HO. This study demonstrates that PTX3 deficiency impairs fracture healing and inhibits traumatic HO, but dose not affect growth plate development in mice. PTX3 expression is up-regulated during chondrocyte matrix synthesis and maturation and is localized in the HA-rich PCM. PTX3 promotes the assembly of HA-rich PCM in a serum- and TSG6-dependent manner, fostering CD44 receptor clustering, activating the FAK/AKT signaling pathway, and promoting chondrocyte matrix synthesis and maturation. Local injection of PTX3/TSG6 matrix protein mixture effectively promotes fracture healing in mice. In conclusion, PTX3-assembled HA-rich PCM promotes chondrocyte matrix synthesis and maturation <em>via</em> CD44/FAK/AKT signaling. This mechanism facilitates EO during fracture healing and traumatic HO in mice.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"192 ","pages":"Article 117385"},"PeriodicalIF":3.5,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NRF2-mediated osteoblast anti-ferroptosis effect promotes induced membrane osteogenesis","authors":"Shuyuan Li ,&nbsp;Shuying Li ,&nbsp;Dawen Yang ,&nbsp;Jingtao Zhang ,&nbsp;Songyang Wang ,&nbsp;Zhanpeng Zeng ,&nbsp;Qunbin Cai ,&nbsp;Qishi Zhou","doi":"10.1016/j.bone.2024.117384","DOIUrl":"10.1016/j.bone.2024.117384","url":null,"abstract":"<div><div>Induced membrane technique (IMT) is a new method for repairing segmental bone defects. However, the mechanism of its defect repair is not clear. In recent years, several studies have gradually indicated that ferroptosis is closely related to bone remodeling. Therefore, this study mainly explored the impact of NRF2-mediated osteoblast anti-ferroptosis on bone mineralization within the induced membrane. Male Sprague-Dawley rats aged 12–14 weeks were randomly divided into four groups (<em>n</em> = 12): Model group, DMF (NRF2 agonist) group, ML385 (NRF2 inhibitor) group and Sham group. Except for Sham group, an IMT model of the right femur was established in all other groups. After 4 weeks and 8 weeks of treatment with DMF and ML385, compared to Model group, DMF group showed significantly higher levels of bone volume fraction (BV/TV), osteogenic factors and NRF2/ARE pathway-related factors (NRF2, GPX4, HO-1 and SLC7A11), while ferroptosis-related indicators (total iron, 4-HNE and MDA) were significantly lower. Conversely, ML385 group exhibited significantly higher ferroptosis-related indicators and lower levels of NRF2/ARE pathway-related factors and osteogenesis. In vitro, erastin could induce ferroptosis in osteoblasts. Compared to Erastin group, Erastin+oe-NRF2 (NRF2 overexpression) group showed significantly increased cell viability, mineralization ability, and levels of NRF2/ARE pathway-related factors, along with reduced ferroptosis effects. However, Erastin+si-NRF2 (NRF2 small interfering) group displayed enhanced ferroptosis effects and significantly reduced cell viability, mineralization ability, and levels of NRF2/ARE pathway-related factors. In conclusion, in the bone grafting area of the induced membrane, there existed ferroptosis caused by iron overload. Activating the anti-ferroptosis effect of osteoblasts mediated by the NRF2/ARE signaling cascade could promote growth and mineralization of bone grafts within the induced membrane.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"192 ","pages":"Article 117384"},"PeriodicalIF":3.5,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901182","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolism-epigenetic interaction-based bone and dental regeneration: From impacts and mechanisms to treatment potential","authors":"Xinyi Chen ,&nbsp;Xiaoyuan Huang ,&nbsp;Xiatong Zhang,&nbsp;Zhuo Chen","doi":"10.1016/j.bone.2024.117382","DOIUrl":"10.1016/j.bone.2024.117382","url":null,"abstract":"<div><div>Metabolic pathways exhibit fluctuating activities during bone and dental loss and defects, suggesting a regulated metabolic plasticity. Skeletal remodeling is an energy-demanding process related to altered metabolic activities. These metabolic changes are frequently associated with epigenetic modifications, including variations in the expression or activity of enzymes modified through epigenetic mechanisms, which directly or indirectly impact cellular metabolism. Metabolic reprogramming driven by bone and dental conditions alters the epigenetic landscape by modulating the activities of DNA and histone modification enzymes at the metabolite level. Epigenetic mechanisms modulate the expression of metabolic genes, consequently influencing the metabolome. The interplay between epigenetics and metabolomics is crucial in maintaining bone and dental homeostasis by preserving cell proliferation and pluripotency. This review, therefore, aims to examine the effects of metabolic reprogramming in bone and dental-related cells on the regulation of epigenetic modifications, particularly acetylation, methylation, and lactylation. We also discuss the effects of chromatin-modifying enzymes on metabolism and the potential therapeutic benefits of dietary compounds as epigenetic modulators. In this review, we highlight the inconsistencies in current research findings and suggest potential approaches to translate fundamental insights into clinical treatments for bone and tooth diseases.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"192 ","pages":"Article 117382"},"PeriodicalIF":3.5,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exogenous bone sialoprotein improves extraction socket healing in Ibsp knockout and wild-type mice","authors":"M.B. Chavez ,&nbsp;N.L. Andras ,&nbsp;M.H. Tan ,&nbsp;T.N. Kolli ,&nbsp;E.Y. Chu ,&nbsp;H.A. Goldberg ,&nbsp;B.L. Foster","doi":"10.1016/j.bone.2024.117381","DOIUrl":"10.1016/j.bone.2024.117381","url":null,"abstract":"<div><div>Bone sialoprotein (<em>Ibsp</em>/BSP) is a bone-associated extracellular matrix protein. <em>Ibsp</em> knockout (<em>Ibsp</em>^{<em>−/−</em>}) mice exhibit defective alveolar bone formation, mineralization, and healing. We hypothesized BSP would rescue defective alveolar bone healing in a molar extraction model in <em>Ibsp</em>^{<em>−/−</em>} mice. Collagen gel with or without native rat BSP (nBSP) or recombinant rat BSP (rBSP) was delivered to sockets after first maxillary molar extraction in <em>Ibsp</em>^{<em>−/−</em>} and wild-type (WT) mice. Tissues were harvested 0, 1, 2, 7, and 14 days post-procedure (dpp) and analyzed by micro-computed tomography, histology, and immunohistochemistry (IHC). Histology and IHC demonstrated that collagen and BSP were retained within sockets. At 14 dpp, both bone volume fraction (BV/TV) and bone mineral density (BMD) were increased by both nBSP (over 50 %) and rBSP (over 60 %), compared to collagen alone in <em>Ibsp</em>^{<em>−/−</em>} mice. In WT alveolar bone, BV/TV and BMD were also increased by nBSP (over 30 %) and rBSP (over 60 %) compared to collagen controls. Gene expression analyses revealed few changes from delivery of nBSP, while addition of rBSP resulted in regulation of cell signaling, ECM, mineralization, and osteoblast/osteoclast-associated genes. Exogenous BSP rescued alveolar bone healing defects in <em>Ibsp</em>^{<em>−/−</em>} mice and enhanced bone healing in WT mice. Despite both forms of BSP improving bone healing, the substantial differences in how they regulate gene expression suggests that exogenous BSP acts in a complex, multifunctional manner to promote bone healing. These results support BSP as a novel approach to improve the quantity and quality of new bone in socket healing.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"192 ","pages":"Article 117381"},"PeriodicalIF":3.5,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142901164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterisation of the influence of dietary fat and sugar on bone health utilising densitometry, micro-computed tomography and histomorphometry","authors":"J. Khan ,&nbsp;H. Sadie-Van Gijsen ,&nbsp;L.M. Kotzé-Hörstmann ,&nbsp;S.H. Kotze ,&nbsp;J.I. Layman-Lemphane","doi":"10.1016/j.bone.2024.117380","DOIUrl":"10.1016/j.bone.2024.117380","url":null,"abstract":"<div><div>Obesogenic feeding can affect systemic metabolism and impact bone health and microarchitecture, but the findings of published studies often appear contradictory. This study aimed to compare the effects of a medium-fat/high-sugar (MF/HS) and a high-fat/high-fructose (HF/Fr) diet on the femora of weanling male Wistar rats, examining bone mineral content and density (BMC, BMD), cortical and cancellous bone microarchitecture and the cell populations within bone. Furthermore, we explored the correlations between circulating bone-targeting factors (in particular leptin, adiponectin and insulin) and bone parameters. Rats were assigned to one of three dietary groups (control: CON; MF/HS: OB1; HF/Fr: OB2; <em>n</em> = 12 each) for 17 weeks. Right-hand side femora were subjected to densitometry to measure BMC and BMD, and micro-computed tomography (μCT) was utilised to assess cortical and cancellous bone. Osteoblast (N.Ob), osteoclast (N.Oc), adipocyte (N.Ad) and chondrocyte numbers (N.Ch) were quantified histomorphometrically. Diet OB1 was largely beneficial to bone, while diet OB2 exerted detrimental effects on BMC, BMD, bone microarchitecture and bone cell populations. In cortical bone, N.Ob was positively correlated with BMD, cortical area and serum leptin. In cancellous bone, N.Ob was positively correlated with serum leptin and BMD, while N.Oc was negatively correlated with serum leptin. Overall, these findings support a role for endogenous circulating leptin in promoting bone formation. We conclude that the impact of different obesogenic diets may be driven by individual dietary effects on circulating factors, which may partly explain the contradictory reports in existing literature on the impact of HF and HS diets on bone.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"192 ","pages":"Article 117380"},"PeriodicalIF":3.5,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142878952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HR-pQCT measurements of changes in periarticular bone density and microarchitecture one year after acute knee injury and after reconstructive surgery","authors":"Nathan J. Neeteson ,&nbsp;Annabel R. Bugbird ,&nbsp;Callie Stirling ,&nbsp;Nina Pavlovic ,&nbsp;Sarah L. Manske ,&nbsp;Richard E.A. Walker ,&nbsp;Steven K. Boyd","doi":"10.1016/j.bone.2024.117376","DOIUrl":"10.1016/j.bone.2024.117376","url":null,"abstract":"<div><div>ACL injuries commonly lead to post-traumatic osteoarthritis (PTOA), but the underlying mechanism is not well-understood. One theorized mechanism is pathological bone remodelling following an ACL tear, for which high-resolution peripheral quantitative computed tomography (HR-pQCT) is uniquely positioned to investigate <em>in vivo</em> in humans. In this study, we longitudinally investigate the one-year changes in periarticular bone density and microarchitecture in the human knee following an ACL tear and reconstructive surgery using data sampled from an on-going observational cohort study. We reduce the number of individual microarchitectural parameters using factor analysis and model one-year changes with mixed-effects models, adjusting for the effects of age, sex, meniscus status, and the baseline microarchitectural state. We find significant evidence of persistent bone density losses one year after both injury and surgery. We also observe significant increases in trabecular separation post-injury, indicating significant structural degradation, and significant increases in subchondral bone plate density post-surgery, a sign of early stiffening. Finally, we observe minimal significant contrasts for the effects of age, sex, and meniscus status, while we observe that the state of the microarchitecture at baseline has significant and varied effects on the subsequent changes, suggesting that the influence of PTOA risk factors on post-injury and post-surgery bone changes may be mediated through the state of the periarticular microarchitecture at injury and/or at surgery. In summary, we found that degradation of periarticular bone microarchitecture was observed post-injury, densification of the subchondral bone plate was observed post-surgery, and the state of the bone microarchitecture at baseline may mediate the influence of PTOA risk factors on post-injury microarchitectural adaptations.</div></div>","PeriodicalId":9301,"journal":{"name":"Bone","volume":"192 ","pages":"Article 117376"},"PeriodicalIF":3.5,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142878956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}