ObjectiveAlterations of the gut microbiota have been implicated in many forms of arthritis, but an examination of cartilage microbial patterns has not been performed. This study was undertaken to characterize the microbial DNA profile of articular cartilage and determine changes associated with osteoarthritis (OA).MethodsWe performed 16S ribosomal RNA gene deep sequencing on eroded and intact cartilage samples from knee OA patients (n = 21 eroded and 21 intact samples) and hip OA patients (n = 34 eroded and 33 intact samples) and cadaver controls (n = 10 knee samples and 10 hip samples). Microbial DNA diversity was assessed, groups were compared, and metagenomic profiles were reconstructed. Confirmation was performed in an independent cohort by clade‐specific quantitative polymerase chain reaction. Findings in human cartilage were compared to those in cartilage from OA‐susceptible C57BL/6 (B6) mice and OA‐resistant MRL/MpJ (MRL) mice. Germ‐free B6 mouse cartilage was analyzed as a methodologic control.ResultsAlpha diversity was reduced in human OA versus control samples (P < 0.0001), and in hip versus knee samples (P < 0.0001). Numerous clades were different in human OA versus control samples, and similar findings were noted in comparisons of murine B6 versus MRL mice. Hip samples were microbiologically distinct from knee samples. OA microbial DNA demonstrated increased gram‐negative constituents (P = 0.02). Functional analysis demonstrated increases in lipopolysaccharide production (P = 9.9 × 10−3), phosphatidylinositol signaling (P = 4.2 × 10−4), and nitrogen metabolism (P = 8 × 10−3) and decreases in sphingolipid metabolism (P = 7.7 × 10−4) associated with OA.ConclusionOur study reveals a microbial DNA signature in human and mouse cartilage. Alterations in this signature, including increases in gram‐negative constituents, occur during the development and progression of human OA. Furthermore, our findings indicate that strain‐specific signatures exist within mouse cartilage that mirror human patterns. Further study of the establishment and potential pathogenic role of these DNA signatures is needed.

The elbow is a complex joint that is the mechanical link in the upper extremity between the hand and the shoulder. Loss of elbow function can severely affect activities of daily living. Arthrodesis of the elbow results in greater functional disability than arthrodesis of the ankle, hip, or knee joints. Arthrodesis is mainly performed for severe joint destruction most commonly due to posttraumatic arthrosis, instability, or infection. The authors describe a new technique of elbow arthrodesis using a step-cut osteotomy that has not been previously reported. They believe that this can increase the surface area for healing with the outcome of a higher fusion rate. It is most important, however, to achieve good compression with lag screws across the fusion site after the desired angled has been achieved. Elbow arthrodesis is not a common orthopedic procedure, but the authors believe that their novel technique provides a reproducible and reliable way to achieve a high fusion rate and desired fusion angle.

Level III, retrospective comparative.

The purpose of this study was to estimate the survivorship of the varus-valgus constrained (VVC) knee implants in primary, aseptic, and septic revision total knee arthroplasty (TKA); determine functional outcomes; main modes of failure; and variables associated with increased mechanical failures. In this study, 685 consecutive cases of primary ( = 247), aseptic ( = 315), and septic revision ( = 123) TKAs with VVC implants were performed between 1999 and 2008; 533 knees (78%) had a mean follow-up of 8.2 years (range, 2-15.1). Kaplan-Meier method was used to evaluate implant survival with mechanical failure as the end point. Clinical outcomes were measured with a modified Knee Society Score (mKSS) and modified Knee Function Score (mKFS) and modes of failure were determined. Cox proportional hazards models were performed to assess for factors associated with implant failure. Ten-year survival was 88.5% (95% confidence interval [CI]: 83.9-93.5%) for primary TKAs, 75.8% (95% CI: 70.4-81.7%) for aseptic, and 54.6% (95% CI: 43.7-68.2%) for septic revisions. Improvement in pre- to postoperative mKSS and mKFS were significant in all three groups ( < 0.05). The most common mode of failure overall was infection. Mechanical modes of failures included periprosthetic fracture (45%) for primary TKA and soft tissue instability (19%) for aseptic revisions. A longer period since the last surgery in affected knee was associated with lower mechanical failures (hazards ratio of 0.55 [95% CI: 0.31-0.95], = 0.03). VVC implant showed reliable survivorship at 10 years although careful patient selection is warranted due to the risk of infection. The main mechanical modes of failure were instability and periprosthetic fracture.

Aging is accompanied by a progressive decline in immune function termed “immunosenescence”. Deficient surveillance coupled with the impaired function of immune cells compromises host defense in older animals. The dynamic activity of regulatory modules that control immunity appears to underlie age-dependent modifications to the immune system. In the roundworm Caenorhabditis elegans levels of PMK-1 p38 MAP kinase diminish over time, reducing the expression of immune effectors that clear bacterial pathogens. Along with the PMK-1 pathway, innate immunity in C. elegans is regulated by the insulin signaling pathway. Here we asked whether DAF-16, a Forkhead box (FOXO) transcription factor whose activity is inhibited by insulin signaling, plays a role in host defense later in life. While in younger C. elegansDAF-16 is inactive unless stimulated by environmental insults, we found that even in the absence of acute stress the transcriptional activity of DAF-16 increases in an age-dependent manner. Beginning in the reproductive phase of adulthood, DAF-16 upregulates a subset of its transcriptional targets, including genes required to kill ingested microbes. Accordingly, DAF-16 has little to no role in larval immunity, but functions specifically during adulthood to confer resistance to bacterial pathogens. We found that DAF-16-mediated immunity in adults requires SMK-1, a regulatory subunit of the PP4 protein phosphatase complex. Our data suggest that as the function of one branch of the innate immune system of C. elegans (PMK-1) declines over time, DAF-16-mediated immunity ramps up to become the predominant means of protecting adults from infection, thus reconfiguring immunity later in life.