What’s New in Musculoskeletal Basic Science

Musculoskeletal injury and disease include >150 distinct conditions affecting joints, bones, ligaments, tendons, muscles, and the spine. Cumulatively, these musculoskeletal disorders represent a substantial global health challenge: in 2020, musculoskeletal disorders were the second-leading cause of non-fatal disability worldwide, affecting >1.63 billion people and becoming the primary contributor to years lived with disability across all populations¹. This burden is particularly pronounced among adults >50 years of age, with higher age-standardized prevalence rates observed in women compared with men². In addition to the impact on individual quality of life, musculoskeletal disorders represent an economic burden that is responsible for global economic losses equivalent to 1.41% of the worldwide gross domestic product in 2021¹.

Systematic epidemiological analyses of the global burden of disease have shown that the trajectory of musculoskeletal disorders is growing at an alarming rate. Since 1990, the prevalence of musculoskeletal disorders has more than doubled, with projections indicating an additional 115% increase by 2050¹. Within the United States alone, >121 million individuals, or approximately one-third of the population, currently have musculoskeletal diseases, accounting for the highest disability rates among all disease categories². Specific conditions demonstrate particularly concerning trends: globally, 595 million people had osteoarthritis in 2020, representing 7.6% of the population and a 132% increase since 1990¹. The rising prevalence of osteoarthritis is attributed to increasing body mass index and the aging population^3,4. Similarly, fracture epidemiology analyses found 178 million acute injuries and 445 million prevalent fractures globally in 2019⁴. With the rapidly expanding aging population, osteoporosis is now estimated to affect >200 million people worldwide, leading to 37 million fragility fractures annually and equating to 70 fractures per minute in the population >55 years of age⁴. By 2050, the worldwide incidence of hip fractures is expected to increase 310% in men and 240% in women, with mortality rates of 20% during the first year^5,6.

Addressing this formidable challenge of musculoskeletal disease burden requires a fundamental commitment to basic science research as the cornerstone of clinical progress. The complexity and heterogeneity of musculoskeletal disorders require sophisticated scientific tools and a deeper mechanistic understanding of the molecular, cellular, and tissue-level processes governing disease pathogenesis, repair, and regeneration. Increased sophistication in both molecular analyses and big data processing has led science into the era of the “omics”⁷. This article highlights how new technology is used in musculoskeletal research to advance our understanding of the molecular and cellular aspects of disease and repair. We also highlight how some research may lead to promising therapeutic avenues.

Novel Outcome Measures in Orthopaedics

Utilizing “Omics” to Enhance Musculoskeletal Disease Diagnosis and Research

Traditional approaches to musculoskeletal disease diagnosis have relied on clinical examination, imaging, and histopathological analysis. These methods have served the field well, but they provide limited insight into the complex molecular mechanisms underlying tissue pathology and healing responses. Although molecular analyses started with simple bulk tissue-level assessments of genes, the field now has advanced tools for performing genomic, transcriptomic, proteomic, epigenomic, and/or metabolomic analyses at a single-cell level with spatial organization, enabling unprecedented data generation. Multiomics is the cutting-edge approach of combining data from multiple “omics” layers to gain a more complete understanding of how systems function. Orthopaedics can capitalize on this gained granularity to improve patient diagnosis and treatment⁷.

The emergence of spatial transcriptomics offers orthopaedic surgeons and researchers a transformative tool that can bridge the gap between molecular biology and clinical practice⁸. Spatial transcriptomics enables simultaneous measurement of gene expression across thousands of genes while preserving the spatial organization of cells within tissue sections^9,10. This capability is particularly relevant for musculoskeletal tissues, in which spatial organization directly influences function. Spatial transcriptomics combines the molecular precision of ribonucleic acid (RNA) sequencing with the spatial context essential for understanding tissue function. This technology can be conceptualized as molecular histology, providing gene expression maps that reveal cellular activity patterns across tissue sections with microscopic resolution. The fundamental principle involves capturing messenger RNA (mRNA) molecules from tissue sections while maintaining information about their spatial coordinates^9,11. Recent technological advances have improved sensitivity^11,12 and accessibility. Integrating spatial transcriptomics into clinical practice requires considering practical factors, including sample collection, processing requirements, turnaround times, and cost considerations. Current protocols can utilize standard formalin-fixed, paraffin-embedded tissue samples, making the technology compatible with existing pathology workflows¹³.

Spatial transcriptomics and other “omics” approaches are revolutionizing our understanding of bone biology⁷. This approach has been used to investigate the niche within bone marrow that harbors mesenchymal stem cells (MSCs)¹⁴, and the skeletal progenitor cells directly within their niche¹⁵. The complex molecular choreography of gradients of gene expression during fracture-healing, underlying bone repair, has been extensively examined¹⁶. The emerging area of mechanomics links local strains to local changes in gene expression¹⁷, which aids understanding of the role of mechanical factors in the molecular regulation of skeletal biology. This spatial molecular mapping has the potential to explain why some fractures heal poorly, despite adequate mechanical stability. Early mesenchymal progenitor cell differentiation can also be studied, providing insights into spatial-temporal mapping during early fracture repair¹⁸

Recent work using spatial transcriptomics combined with single-cell nuclear sequencing and lineage tracing has dramatically increased the understanding of pseudarthrosis after fracture in patients with inactivating mutations in the neurofibromatosis type 1 (NF1) gene and illustrates the power of these approaches. Spatial transcriptomics, combined with other analyses, using tissues derived from animal models and patients, revealed that the bone morphogenetic protein (BMP) pathway was not activated in pseudarthrosis tissue but that increased mitogen-activated protein kinase (MAPK) signaling was apparent in fibrotic tissue¹⁶. This suggests a failure to activate the skeletogenic program in the fibrotic tissues. Interestingly, skeletal progenitor cells and Schwann cells harboring mutations that inactivate both alleles of NF1 are present in patient-derived pseudarthrosis samples. The Schwann cells appear to potentiate this pathology by maintaining the skeletal progenitor cells in a fibrotic state via paracrine activities that increase MAPK signaling instead of allowing their transition to skeletal cell types¹⁹. Results from studies like these could lead to highly targeted patient or disease-specific therapeutics.

Spatial transcriptomics is enhancing bone tumor diagnosis by revealing molecular signatures that complement traditional histopathological analysis²⁰. Bone tumors that appear histologically similar exhibit distinct molecular profiles that may require different treatment approaches. The technology may be particularly valuable for analyzing tumor heterogeneity within individual samples and guiding the development of targeted therapies.

Osteoarthritis has long been recognized as a heterogeneous disease, and “omics” may help to identify the molecular basis of this heterogeneity^21,22. Cartilage samples from osteoarthritic joints show distinct molecular zones, including areas of attempted repair with high anabolic gene expression, regions of active degradation with elevated catabolic enzymes, and zones of cellular senescence with inflammatory signaling²³. Going one step further, spatial mass spectrometry has been used to assess protein modifications in patients with osteoarthritis. This work has shown that alterations in N-glycosylation may contribute to pathological changes in these patients²⁴. We may now also be able to use multiomics techniques to understand a link to pain phenotypes in osteoarthritis²⁵.

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The next generation of “omics” research combines spatial transcriptomics and mechanomics in fracture repair. As Mathavan et al. showed, this technique may have broad applications in furthering our understanding of osteoarthritis, fragility fractures, or even peri-implant fractures¹⁷.

Schwann cells contribute to pseudarthrosis in patients with mutations in NF1. Research such as articles by Rios et al.¹⁶ and Perrin et al.¹⁹ has suggested MEK-SHP2 pathway inhibition as a target to prevent fibrous nonunion.

New research, such as that by Collins et al.²⁵, has provided evidence that the soluble cytokines leptin and adipsin (or complement factor D) from adipose tissue outside the joint independently regulate cartilage damage and pain in osteoarthritis. This new mechanistic link creates novel druggable molecular targets that could prevent or treat obesity-related osteoarthritis by addressing a root systemic cause of the disease.

Biomarkers in Musculoskeletal Disease and Injury

The diagnostic and clinical utility of biomarkers that are standard in oncology has motivated the quest for quantitative biomarkers in other fields to detect disease progression or guide therapeutic decision-making earlier than current clinical standards allow. The U.S. Food and Drug Administration (FDA) has defined a biomarker as a “characteristic that is measured as an indicator of normal biological processes, pathological processes, or responses to an exposure or intervention”²⁶. To date, biomarkers have not meaningfully influenced clinical practice in orthopaedics. Emerging research efforts aim to address this shortcoming by identifying novel molecular targets for musculoskeletal biomarkers and expanding testing into larger sample sizes to lay the groundwork for meaningful clinical adoption.

Systematic analyses of osteoarthritis biomarkers reveal a modern approach to improving diagnostic accuracy by targeting multiple molecular levels to integrate inflammatory, proteomic, and metabolite markers²⁷. This integrated approach also aims to bring in more diversity with new targets. For example, although inflammatory biomarkers have traditionally focused on interleukins (interleukin [IL]-6, IL-7, IL-1β), tumor necrosis factor (TNF)-α, and nuclear factor (NF)-κβ, emerging research has identified the carbohydratebinding protein galectin²⁸ and the hormone adiponectin produced by fat cells²⁹ as inflammatory regulatory molecules that are positively associated with osteoarthritic degradation and pain. These markers represent a shift toward understanding the complex inflammatory networks underlying joint pathology.

An alternative approach gaining momentum is to understand the potential diagnostic or prognostic utility of measuring cellular senescence within the immune cells³⁰. The senescence-associated secretory phenotype (SASP) has significant overlap with traditional inflammatory markers, but now, in addition to measuring pro-inflammatory cytokines, flow cytometry has been used at a clinical scale to measure 5-Dodecanoylaminofluorescein di-β-D-Galactopyranoside (C₁₂ FDG), which is a lipophilic compound that fluoresces when hydrolyzed by senescence-associated β-galactosidase activity³¹. Specifically, in a study of aging and osteoarthritis, C₁₂FDG⁺ peripheral blood mononuclear cells and T cells were significantly elevated in patients with mild to moderate osteoarthritis compared with healthy subjects, providing a quantifiable clinical tool to assess cellular senescence associated with osteoarthritic pathogenesis³².

In parallel, inflammatory biomarkers have gained clinical momentum in fracture repair based on the principle of “inflammaging,” which has become a well-established research term to describe the pro-inflammatory immunological shift that occurs with aging³³. Pro-inflammatory macrophage phenotypes have emerged as critical negative biomarkers of fracture-healing at a preclinical level^34,35. Additionally, neutrophils and neutrophil extracellular traps have been identified as both diagnostic biomarkers and therapeutic targets for heterotopic ossification detection and mitigation, expanding the clinical utility of immune-based preclinical assessments³⁶. At a clinical level, research has identified that terminally differentiated peripheral CD8⁺ T (T_EMRA) cells correlate strongly with delayed fracture-healing³⁷. Recent prospective analysis of mandibular fracture-healing confirmed the prognostic capability of CD8⁺ T_EMRA to CD4⁺ regulatory T cell (T_reg) imbalance, establishing immune profiling as a predictive tool for healing complications³⁸.

In addition to immune biomarkers, matrix molecules remain traditional candidates for orthopaedic biomarkers, given their prominence in musculoskeletal tissues and the inherent link of tissue remodeling with inflammatory disease and tissue repair. For example, bone turnover markers characterizing osteoblast and osteoclast activity have gained some clinical traction as a complement to bone mineral density testing in osteoporosis monitoring³⁹. Bone turnover markers have recently been repurposed in fracture studies, in which they have shown a positive correlation with radiographic evidence of healing at 12 weeks after the fracture, providing earlier indicators of repair progression than traditional imaging alone⁴⁰. Among emerging methods, a biomarker of endochondral bone turnover, specifically the degradation product of collagen X marker (CXM), represents a recent advancement in fracture assessment. Recent clinical studies have shown that CXM peaks approximately 25 days after a fracture, markedly earlier than radiographic evidence of healing, and that patients who have early fracture-healing show peak CXM values at 6 weeks that are significantly higher than those of patients who have standard healing patterns⁴¹. This groundwork enables future studies to define the utility of CXM in detecting delayed union and nonunion before radiographic evidence becomes available.

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Incorporating biomarkers to specialized T-cells^37,38 and/or the endochondral phase of fracture-healing⁴¹ may create opportunities to identify poorly healing fractures earlier than previously possible.

Emerging Therapeutic Strategies

Mitochondrial Transfer

Mitochondrial transfer is an emerging therapeutic strat egy that involves the transfer of mitochondria from donor cells to recipient cells, aiming to restore mitochondrial function and improve cellular health. This process has shown promise in various medical fields, including orthopaedics. Mitochondrial transfer has been shown to increase adenosine triphosphate production, restore mitochondrial function, and reduce apoptosis in injured cells⁴². Mitochondrial transfer can occur through several mechanisms, including tunneling nanotubes, extracellular vesicles, and direct cell-to-cell contact^43–46. Bone marrow MSCs are frequently used as donor cells because of their ability to donate healthy mitochondria and promote tissue repair^43,46. Mitochondria have been shown to play a crucial role in bone health by regulating cell differentiation, energy production, and osteogenesis. Dysfunction of mitochondria is linked to orthopaedic disorders such as osteoporosis and osteoarthritis, contributing to impaired bone homeostasis and increased fracture risk⁴⁷. Emerging strategies include mitochondrial biogenesis stimulation, fission inhibition, and direct mitochondrial transplantation, which have shown potential in enhancing bone repair and reducing oxidative stress⁴⁷.

In osteoarthritis, mitochondrial transfer has been shown to improve mitochondrial function in chondrocytes, reducing oxidative stress, inflammation, and apoptosis, which are critical factors in the progression of osteoarthritis^42,48. Some studies have indicated that mitochondrial transfer can improve key aspects of chondrocyte dysfunction in inflammatory osteoarthritis models, supporting its therapeutic potential for treating or slowing osteoarthritis^42,48. Specifically, mitochondrial transfer from MSCs to chondrocytes may enhance cellular function and slow down or reverse cartilage degeneration^46,48. Similarly, mitochondria transferred from bone marrow MSCs to injured tenocytes have shown decreased apoptosis, promoted proliferation, and restored mitochondrial function, thereby improving tendon healing⁴⁹. This transfer of healthy mitochondria from MSCs further helped to reduce oxidative stress and inflammation, which is crucial for tendon repair⁴⁹.

Although the therapeutic potential of mitochondrial transfer is evident, the precise mechanisms and regulatory factors involved in mitochondrial transfer need further elucidation⁴⁶. There are still challenges to be overcome, including safety concerns, immune response, genetic changes, dosage optimization, and quality control⁵⁰.

There is also a need to address ethical challenges and policy barriers to allow mitochondrial transfer techniques to provide treatment for individuals affected by orthopaedic conditions⁵¹. Current clinical applications have focused on the delivery of autologous mitochondria to limit potential immune responses and rejection of donor mitochondria⁵². More research is required to translate these findings into clinical practice, ensuring the safety and efficacy of mitochondrial therapy in orthopaedic treatments^{47 ,49}. Mitochondrial transfer holds promise for treating various orthopaedic conditions by restoring mitochondrial function and improving cellular health.

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Mitochondrial transfer is clinically relevant because it restores cellular function in damaged tissues by increasing adenosine triphosphate (ATP) production, reducing oxidative stress and apoptosis, and promoting tissue repair, particularly in orthopaedic conditions such as osteoarthritis and tendon injuries where mitochondrial dysfunction is emerging as a key driver of disease progression. Recent research⁴⁶ has identified that the connexin 43 isoform GJA1–20k is a critical regulator of mitochondrial transfer from mesenchymal stromal cells to chondrocytes, with overexpression of GJA1–20k significantly increasing transfer efficiency and presenting a promising therapeutic target for enhancing cartilage repair in osteoarthritis.

Therapies to Address Orthopaedic Infection

Complications of orthopaedic infections present clinical challenges that increase morbidity and health-care costs and often lead to poor patient outcomes^53–55. Developing alternatives to antibiotics is crucial to reducing antibiotic resistance and facilitating antibiotic stewardship^56–58. Efforts in this area are multifaceted, including targeting biofilm formation and maturation on implants and persistent infection directly within bone.

Infections after orthopaedic surgery can be catastrophic and may arise from implants, during surgery, or due to the nature of the injury. Infections can be established directly within the bone⁵⁹ or on surfaces, such as on implants, via biofilm formation⁶⁰. Biofilm formation is particularly problematic in patients with orthopaedic trauma⁶¹. Biofilms are microbial communities that form on surfaces and facilitate immune evasion by the bacteria by creating an extracellular matrix in which the bacteria thrive and persist. During biofilm formation, bacteria first adhere to the surface of materials and form microcolonies. These colonies mature and eventually disperse bacteria to seed other surfaces. Treating patients with a periprosthetic joint infection involves debridement of the infected tissue and removal of the implant, followed by placing a new implant into the patient. However, due to a high reinfection rate, research to develop treatments for these scenarios is underway and focuses on disrupting biofilm formation, maturation, or dispersion.

One opportunity is the development of implants that have antibacterial properties that are not cytotoxic to the mammalian cells that need to colonize the implant surface to ensure osseointegration⁶². Because of the regulatory challenges associated with incorporating these coatings onto implants, topically applied treatments at the time of surgery are gaining interest. An alternative may be to use materials that are made in ways that resist biofilm formation and are not surface-modified⁶³, but these need further optimization, coupled with rigorous in vivo testing.

One intriguing approach to treat postoperative orthopaedic infections may be to target bacteria directly using bacteriophages that infect and kill the bacteria themselves. Phages were initially studied in a rat model of implant infection, and, when combined with antibiotics, they eliminated biofilms⁶⁴. However, subsequently, phage-resistant bacteria emerged in many studies attempting to treat infections with this approach, including in human trials⁶⁵.

Despite potential limitations, interest in phage therapy as an adjunctive treatment for difficult orthopaedic infections has increased over the past decade, driven by the rise of antibiotic resistance and the challenges associated with biofilm formation in chronic wounds and periprosthetic joint infections^66,67. Phage therapy, which utilizes bacteriophages to target and kill specific bacterial pathogens, has shown promising results in various preclinical and clinical settings, including in the treatment of periprosthetic joint infections and fracture-related infections^68,69.

Case reports have demonstrated the potential of phage therapy to improve outcomes in patients with chronic orthopaedic infections^70,71. Additionally, personalized phage therapy combined with antibiotics has been successful in eradicating infections caused by multidrug-resistant pathogens, as evidenced by a case of chronic periprosthetic joint infections treated with phage therapy and meropenem, resulting in no infection relapse after 2 years⁷¹.

Despite these promising results, several challenges remain, including optimal dosing strategies, understanding phage pharmacokinetics, and addressing bacterial heterogeneity within infections. Moreover, the development of phage delivery systems, such as phage-loaded hydrogels and biodegradable orthopaedic implants, is crucial to enhance the efficacy and safety of phage therapy^68,72. Future research should focus on large-scale, randomized controlled trials to validate the clinical efficacy and safety of phage therapy and explore phage engineering and innovative delivery systems to broaden its applicability. Overall, phage therapy holds potential as a complementary treatment for orthopaedic infections, offering a targeted approach to combat antibiotic-resistant bacteria and biofilm-associated infections.

In addition to phage therapy, using MSCs as an adjunct to conventional antibiotic therapy has recently received attention outside of the field of orthopaedics. The secretome of MSCs has long been established as bioactive with applications in regenerative medicine⁷³, but recently there has been increased interest in the ability of these cells to secrete antimicrobial peptides, including lipocalin 2, cathelicidin, β-defensin 2, and hepcidin^74–76. Data have supported that human MSCs possess direct antibacterial properties, can augment host immune defense mechanisms, and may disrupt bacterial biofilms⁷⁶. MSCs have been utilized in multiple clinical trials as a solution to disease caused by graft versus host disease⁷⁷. Capitalizing on these research advances and the mechanism of action data for treating orthopaedic infection could hold great promise.

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Orthopaedic infections remain an important clinical problem and novel approaches are needed to improve outcomes. Translating concepts related to the antimicrobial capacity of stem cells over to orthopaedic applications^75,76 or creating biodegradable implants containing bacteriophages to fight methicillin-resistant Staphylococcus aureus emerge as next-generation technologies⁷².

Next-Generation Gene Therapy

Modern approaches to gene activation have also gained momentum in the research literature following the success of the mRNA-based COVID-19 vaccines^78,79. mRNA therapeutics deliver a template for the endogenous production of proteins over the time course of days to weeks, which offers the benefit of cells using native post-translational modification infrastructure that may improve the function of the protein and address the short half-life of recombinant proteins that have been developed as drugs. Unlike traditional DNA-based gene therapy, mRNA does not integrate into the genome, so there is no risk of insertional mutagenesis or permanent genetic alterations. Advances in RNA biology, such as the inclusion of modified RNA nucleosides, have significantly increased protein translation and extended the expression kinetics⁸⁰, but there remain few regenerative medicine applications⁸¹.

Only a few pioneering studies have developed RNA-based therapeutics for orthopaedic applications in the last few years, with initial projects generally focused on encoding for BMP-2 or BMP-9, transfected by loading the mRNA onto various implantable scaffolds^82–85. The seminal efficacy study using chemically modified mRNA encoding BMP-2 demonstrated that large defects were healed efficiently and that the mRNA therapeutic specifically promoted a more native endochondral bone repair when compared with recombinant human BMP⁸⁶; this is promising, as the protein has fallen out of favor clinically for applications in fracture repair because of safety concerns and poor-quality bone formation⁸⁷.

Recently, mRNA was also used as a therapeutic to activate the Wnt signaling pathway, showing that a constitutively active β-catenin sequence could accelerate fracture-healing when delivered locally by injection to the fracture callus⁸⁸. The lipophilic nature of the Wnt protein has made it a challenging pathway to directly activate using traditional technology, resulting in clinically available drugs targeting the Wnt inhibitors through monoclonal antibodies to activate the pathway indirectly⁸⁹. These studies exemplify how mRNA therapeutics may promote bone repair in a fashion that more accurately reflects the endogenous healing pathway and may help to diversify the therapeutic targets for different aspects of repair.

Successful RNA therapeutics depend heavily on encapsulation in lipid nanoparticles to facilitate cellular uptake and to protect the RNA from degradation. Most lipid nanoparticles have been designed for systemic delivery for applications such as vaccines. Advances in local delivery also help to create a more robust toolbox for the regenerative application of mRNA for musculoskeletal disorders. For example, biomimetic mineralized microparticles and nanoparticles can achieve and extend local lipid nanoparticle-encapsulated mRNA or provide stabilization of the RNA for extended storage^90–93.

Alternatively, biomimetic lipid nanoparticles may provide tissue homing capabilities. Macrophage-inspired lipid nanoparticles are an example of this possibility, in which the cell membrane proteins from macrophages are incorporated into the lipid nanoparticles to facilitate self-tolerance in order to evade immune clearance and adhesion to inflamed vasculature^94–97. In a study to test orthotopic homing, these macrophage-inspired lipid nanoparticles, or “orthosomes,” target articular cartilage trauma after systemic administration⁹⁸. The rapid advancement of RNA and nanoparticle engineering will lay the foundation for translational technologies that could be optimized for various musculoskeletal disorders.

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Regenerative RNA therapeutics emerging in musculoskeletal research have demonstrated the capacity to reduce cartilage fibrosis in osteochondral defects⁹³, achieve tissue-specific targeting following injury⁹⁸, promote bone repair^86,88, and provide solutions to long-term storage stability⁹⁰.

Conclusion

Musculoskeletal diseases contribute to individual and societal socioeconomic burdens worldwide. Current health-care delivery models underutilize promising therapeutic approaches, including advanced pharmacological interventions, regenerative medicine technologies, and digital health solutions incorporating artificial intelligence. Collaborative interdisciplinary approaches will continue to be essential for developing, adopting, and implementing new methodologies to diagnose, treat, and measure outcomes. The emergence of biomarkers, advanced therapeutic strategies, and personalized treatment algorithms will ultimately improve patients’ function throughout their lifetimes.

Upcoming Meetings and Events Related to Orthopaedic Basic Science.

• The Gordon Research Conference Bones and Teeth will be held from January 25 to 30, 2026, in Grand Galvez, Galveston, Texas, United States.

• The Annual Meeting of the Orthopaedic Research Society (ORS) will be held from March 27 to 31, 2026, in Charlotte, North Carolina, United States.

• The Annual Meeting of the Osteoarthritis Research Society International (OARSI) World Congress on Osteoarthritis will be held from April 23 to 26, 2026, in West Palm Beach, Florida, United States.

• The ORS International Section of Fracture Repair Biennial Meeting will be held from May 6 to 8, 2026, in Berlin, Germany.

• The AO Research Institute Orthopaedics Meeting, Cartilage and Disc, will be held from June 22 to 24, 2026, in Davos, Switzerland.

• The Annual Meeting of the International Society for Stem Cell Research will be held from July 8 to 11, 2026, in Montreal, Canada.

• The Gordon Research Conference on Musculoskeletal Biology and Bioengineering will be held from August 2 to 7, 2026, at Proctor Academy in Andover, New Hampshire, United States.

• The Orthopaedic Trauma Association (OTA) Basic Science Focus Forum will be held on September 23, 2026, in Nashville, Tennessee, United States.

• The Annual Meeting of the European Orthopaedic Research Society (EORS) will be held from September 23 to 25, 2026, in Madrid, Spain.

• The Annual Meeting of the American Society for Bone and Mineral Research (ASBMR) will be held from October 9 to 12, 2026, in Boston, Massachusetts, United States.