Jonathan James Huang

Background: Knee injuries among older adults carry disproportionate clinical consequences, since diminished bone quality and comorbidities can transform a routine sprain into a sentinel event for functional decline. Physical activity is essential to healthy aging but may also contribute to musculoskeletal injury. National data describing recreational activities associated with geriatric knee injuries and injury characteristics remain limited.Methods: This retrospective cohort study queried the National Electronic Injury Surveillance System (NEISS) for patients aged 65+ years presenting to United States emergency departments with knee injuries related to recreational and exercise activities from 2016 to 2025. National estimates (NEs) were calculated using NEISS sample weights and stratified by sex, age, activity, diagnosis, and hospitalization status.Results: An estimated 193,590 geriatric knee injuries were identified. Males accounted for 51.54% of injuries and females for 48.46%. Most injuries occurred among patients aged 65-74 years (63.46%). Injuries increased significantly over the study period (p < 0.001) Strain or sprain was the most common diagnosis across nine of ten most common activities, while bicycling was characterized primarily by contusion or abrasion (24.3%). Skiing carried the highest hospitalization proportion and bowling the lowest. Exercise without equipment and bicycling accounted for the largest share of injuries across sex and age strata.Conclusion: Geriatric knee injuries related to recreational activity have increased significantly, concentrated in low and moderate impact activities such as walking based exercise and bicycling, with meaningful variation in hospitalization risk. These findings support activity specific counseling tailored to recreational behaviors prevalent among older adults.

Aging exacerbates the incidence of discogenic chronic low back pain by excessive inflammation and immune cell presence. Aging reduces intervertebral disc (IVD) Wnt signaling, which is associated with IVD cell differentiation, IVD cell proliferation and anti‐inflammatory signaling. However, it is unclear how in vivo Wnt signaling‐absent IVD cells, which model aged IVD cells, regulate chemotactic signaling and immune cell recruitment. We hypothesized that Wnt signaling‐absent IVD cells attenuate chemotactic transcription and immune cell recruitment to naive IVD and in response to IVD injury. First, because aging reduces Wnt signaling in all IVD cells, we deleted β‐catenin using the AcanCreERT2. β‐catenin deletion reduced monocyte chemoattractant protein‐1 (MCP1/CCL2) Ccl2 in male and female IVDs by 58% and 79%, respectively ( n = 5–6/sex). Using positron emission tomography/computed tomography (PET/CT) imaging of myeloid cells in 5‐month‐old mice ( n = 4 IVD/sex/grp), deletion of β‐catenin reduced myeloid‐derived cell burden in naive IVD by 79% and attenuated IVD injury‐induced recruitment by 48%. Next, because nucleus pulposus (NP) cells begin losing Wnt signaling early in life, we deleted β‐catenin using the ShhCreERT2. Compared to RNA‐sequencing of WT IVD post injury ( n = 3/grp), deletion of β‐catenin in NP cells impaired the activation of immune cell pathways, such as MCP1/CCL2. Together, the chemotactic transcriptomic response and myeloid cell accumulation due to IVD injury were impaired by the absence of IVD Wnt signaling transcription cofactor β‐catenin . These data suggest that low‐grade IVD inflammation and chronic IVD immune cell accumulation in aged IVD cells are regulated by IVD Wnt signaling.

Background: Modic changes (MC) are painful vertebral bone marrow lesions. Three interconvertible types represent different pathology stages with MC1 being the most painful, MC2 less painful, and MC3 asymptomatic. Bacterial ( Cutibacterium acnes ( C. acnes )–mediated) and non‐bacterial etiologies are both suggested to induce MC1, but it remains unclear whether MC conversion is etiology‐specific. This has important implications for patient management and the development of MC therapies. Aims: To assess MC‐subtype lesion prevalence and pain‐like behavior over time in an etiology‐specific MC rat model. Methods: Four‐to‐five‐month‐old Sprague–Dawley rats underwent sham ( n = 12) surgery or endplate injury followed by an intradiscal injection of 2.5 μL of either TNF‐α (1000 ng/mL PBS) ( n = 19) or C. acnes (3.2 × 10 ⁸ CFU/mL in PBS) ( n = 18) to mimic aspects of bacterial versus non‐bacterial MC etiologies. MC‐subtype prevalence was evaluated by magnetic resonance imaging at 1, 8, and 14 weeks post‐injury. Disc degeneration, bone marrow lesion neutrophil elastase and CD19 immunoreactivity, spinal cord sensitization, and pain‐like behavior (von Frey) were assessed, and contributors to pain‐like behavior were identified (random forest). Results: C. acnes injection caused higher MC1‐like lesion prevalence than TNF‐α and Sham at all‐time points and higher spinal cord substance P expression at 14 weeks post‐injury. MC2‐like lesions increased over time in TNF‐α‐injected discs and were more prevalent at 14 weeks post‐injury than C. acnes . C. acnes injection resulted in bone marrow lesions with higher neutrophil elastase‐ and CD19 immunoreactivity. MC1‐like lesions contributed strongest to pain‐like behavior, although von Frey did not differ between groups. Conclusion: Intradiscal C. acnes injection sustained MC1‐like lesions in an etiology‐specific lumbar MC rat model, suggesting that patients with bacterial MC etiology may be more likely to persist in painful MC1.

Randomized controlled trials (RCTs) are essential for guiding the treatment of vertebral compression fractures with kyphoplasty, yet the statistical robustness of their findings has not been thoroughly evaluated. This systematic review assessed the fragility of dichotomous outcomes in kyphoplasty RCTs using the fragility index (FI), reverse fragility index (rFI), and fragility quotient (FQ). A comprehensive search of PubMed, Embase, and MEDLINE identified eligible RCTs, yielding 282 dichotomous outcomes for analysis. The overall median FI was 4 (interquartile range [IQR], 4-5), corresponding to a median FQ of 0.020 (IQR, 0.013-0.040). Statistically significant outcomes (n=18) demonstrated greater fragility, with a median FI of 2 (IQR, 1-4) and FQ of 0.015 (IQR, 0.011-0.029), compared with nonsignificant outcomes (n=264; FI, 5 [IQR, 4-5]; FQ, 0.020 [IQR, 0.013-0.041]). Subgroup analyses revealed that pain and complication outcomes had median FIs of 4 and 5, respectively, with FQs ranging from 0.016 to 0.025. Cement leakage outcomes were the most fragile (FI, 4; FQ, 0.048). More than half of the analyzed outcomes involved a greater number of patients lost to follow-up than their corresponding FI, underscoring the need for cautious interpretation of kyphoplasty trial results and supporting the inclusion of fragility metrics in future trial reporting to better inform clinical decision-making.

Background: Intervertebral disc (IVD) degeneration (IVDD) is a major cause of global disability. Three papers on puncture models of IVDD were published 20 years ago, transforming the application of preclinical animal models for pathophysiology and therapeutic screening studies. Methods: Narrative review describing historic and current usage of preclinical puncture models of IVDD, documenting their introduction to induce slow, progressive IVDD and evolution to include many injury types broadly called “puncture models.” IVDD puncture models were reviewed for variability in species, needle gauge, puncture depth, IVD compartment, injectates, angle of puncture, motion of needle, and IVDD phenotype mimicked. Results: IVD puncture models gained prominence following seminal 2005 publications describing needle puncture to induce slow, progressive IVDD for screening therapies. Specific details of puncture methods were described for controlling injury severity to induce IVDD phenotypes, including slow progressive IVDD, severe IVDD, chronic IVDD, disc herniation, and Modic‐like changes. Common measurements for characterizing IVDD were also described. Conclusions: Surgically induced IVD puncture injury animal models have evolved over decades to include many variations simulating distinct clinical phenotypes of IVDD. To facilitate cross‐study comparisons, we recommend reporting a common set of injury features including needle gauge, puncture depth, injectates, puncture angle changes, needle motion, involvement of endplate and surrounding tissues, and phenotypes of IVDD mimicked. Surgically induced “outside‐in” puncture injury models are valuable tools to test specific hypotheses and screening therapies.