To determine the role of magnetic resonance imaging (MRI) MOCART (Magnetic Resonance Observation of Cartilage Repair Tissue) 1 and 2.0 scores in the assessment of postoperative outcome after autologous matrix-induced chondrogenesis (AMIC) for the treatment of osteochondral lesions of the talus (OLTs). It was hypothesized that preoperative patient factors or OLT morphology are associated with postoperative MOCART scores; yet postoperative clinical outcome is not. Cohort study; Level of evidence, 4. This study evaluated isolated AMIC that were implanted on the talus of 35 patients for the treatment of symptomatic OLT. Tegner and AOFAS (American Orthopaedic Foot and Ankle Society) scores were obtained at an average follow-up of 4.5 ± 1.8 years and postoperative MRI scored according to the MOCART 1 and 2.0. OLT size showed significant correlation with postoperative MRI scores (MOCART 1: P = 0.006; MOCART 2.0: P = 0.004). Bone grafting was significantly associated with a MOCART 1 subscale (signal intensity of repair tissue; P = 0.038). Age and defect size showed significant correlations with MOCART 2.0 subscales (P < 0.05). Patients with shorter follow-up had a significantly higher MOCART 1 score and a trend toward better MOCART 2.0 scores than patients with longer follow-up (64.7 vs. 52.9 months, P = 0.02; 69.4 vs. 60.6 months, P = 0.058). No MOCART score was associated with postoperative patient-reported outcomes (n.s.). Osteochondral lesion size is associated with postoperative MOCART scores in patients treated with AMIC for OLTs, with decreasing MOCART scores over time. Yet clinical outcome does not correlate with any MOCART score. Thus, MOCART assessment seems to have no significant role in the postoperative treatment of asymptomatic patients that underwent AMIC for OLTs.

Focal nerve injuries are often associated with neuropathic pain. Preclinical research suggests altered neuroimmune signalling underlies such neuropathic pain; however, its cause remains poorly understood in humans. In this multicentre cohort study, we describe the local cellular and molecular signature of neuropathic pain at the lesion site, using Morton's neuroma as a human model system of neuropathic pain (n = 22; 18 women) compared with nerves from participants without nerve injury (n = 11; 4 women). Immunofluorescent staining revealed demyelination and chronic infiltration of immune cells in Morton's neuroma. RNA bulk sequencing identified 3349 differentially expressed genes between Morton's neuroma and controls. Gene ontology enrichment analysis and weighted gene co-expression network analyses revealed modules specific for host defence and neurogenesis. Deconvolution analysis confirmed higher densities of macrophages and B cells in Morton's neuroma than control samples. Modules associated with defence response, neurogenesis, and muscle system development as well as macrophage cell populations identified by deconvolution correlated with patients' paroxysmal or evoked pain. Of note, we identified a consistently differentially expressed gene signature (MARCO, CD163, STAB1), indicating the presence of a specific M(GC) subset of macrophages. MARCO gene expression correlated with paroxysmal pain. Targeted immunofluorescent analyses confirmed higher densities of intraneural CD163⁺MARCO⁺ macrophage subsets in Morton's neuroma. Our findings provide detailed insight into the local molecular signature in the context of human focal nerve injury. There is clear evidence for an ongoing role of the immune system in chronic peripheral neuropathic pain in humans, with macrophages and specifically the M(GC) MARCO⁺ subset implicated.

We determined antibodies to the pandemic influenza A (H1N1) 2009 virus in children to assess: the incidence of (H1N1) 2009 infections in the 2009/2010 season in Germany, the proportion of subclinical infections and to compare titers in vaccinated and infected children. Eight pediatric hospitals distributed over Germany prospectively provided sera from in- or outpatients aged 1 to 17 years from April 1^st to July 31^st 2010. Vaccination history, recall of infections and sociodemographic factors were ascertained. Antibody titers were measured with a sensitive and specific in-house hemagglutination inhibition test (HIT) and compared to age-matched sera collected during 6 months before the onset of the pandemic in Germany. We analyzed 1420 post-pandemic and 300 pre-pandemic sera. Among unvaccinated children aged 1–4 and 5–17 years the prevalence of HI titers (≥1∶10) was 27.1% (95% CI: 23.5–31.3) and 53.5% (95% CI: 50.9–56.2) compared to 1.7% and 5.5%, respectively, for pre-pandemic sera, accounting for a serologically determined incidence of influenza A (H1N1) 2009 during the season 2009/2010 of 25,4% (95% CI : 19.3–30.5) in children aged 1–4 years and 48.0% (95% CI: 42.6–52.0) in 5–17 year old children. Of children with HI titers ≥1∶10, 25.5% (95% CI: 22.5–28.8) reported no history of any infectious disease since June 2009. Among vaccinated children, 92% (95%-CI: 87.0–96.6) of the 5–17 year old but only 47.8% (95%-CI: 33.5–66.5) of the 1–4 year old children exhibited HI titers against influenza A virus (H1N1) 2009. Serologically determined incidence of influenza A (H1N1) 2009 infections in children indicates high infection rates with older children (5–17 years) infected twice as often as younger children. In about a quarter of the children with HI titers after the season 2009/2010 subclinical infections must be assumed. Low HI titers in young children after vaccination with the AS03_B-adjuvanted split virion vaccine need further scrutiny.

Charcot neuropathic arthropathy (CN) is a chronic, progressive, destructive, non-infectious process that most frequently affects the bone architecture of the foot in patients with sensory neuropathy. We evaluated the outcome of protected weightbearing treatment of CN in unilaterally and bilaterally affected patients and secondarily compared outcomes in protected versus unprotected weightbearing treatment. Patient records and radiographs from 2002 to 2012 were retrospectively analyzed. Patients with Type 1 or Type 2 diabetes with peripheral neuropathy were included. Exclusion criteria included immunosuppressive or osteoactive medication and the presence of bone tumors. Ninety patients (101 ft), mean age 60.7 ± 10.6 years at first diagnosis of CN, were identified. Protected weightbearing treatment was achieved by total contact cast or custom-made orthosis. Ulcer, infection, CN recurrence, and amputation rates were recorded. Mean follow-up was 48 (range 1–208) months. Per the Eichenholtz classification, 9 ft were prodromal, 61 in stage 1 (development), 21 in stage 2 (coalescence) and 10 in stage 3 (reconstruction). Duration of protected weightbearing was 20 ± 21 weeks and 22 ± 29 weeks in patients with unilateral and bilateral CN, respectively. In bilaterally affected patients, new ulcers developed in 9/22 (41%) feet. In unilaterally affected patients, new ulcers developed in 5/66 (8%) protected weightbearing feet and 4/13 (31%) unprotected, full weightbearing feet (p = 0.036). The ulceration rate was significantly higher in bilaterally versus unilaterally affected patients with a protected weightbearing regimen (p = 0.004). Soft tissue infection occurred in 1/13 (8%) unprotected weightbearing feet and 1/66 (2%) protected weightbearing feet in unilaterally affected patients, and in 1/22 (4%) protected weightbearing feet of bilaterally affected patients. Recurrence and amputation rates were similar across treatment modalities. Bilateral CN results in significantly more ulcers than unilateral CN and leads to slightly higher soft tissue infections. Protected weightbearing in an orthopedic device can reduce the risk for complications in acute CN of the foot and ankle.

Surgical site infection (SSI) after elective orthopedic foot and ankle surgery is uncommon and may be higher in selected patient groups. Our main aim was to investigate the risk factors for SSI in elective orthopedic foot surgery and the microbiological results of SSI in diabetic and non-diabetic patients, in a tertiary foot center between 2014 and 2022. Overall, 6138 elective surgeries were performed with an SSI risk of 1.88%. The main independent associations with SSI in a multivariate logistic regression analysis were an ASA score of 3–4 points, odds ratio (OR) 1.87 (95% confidence interval (CI) 1.20–2.90), internal, OR 2.33 (95% CI 1.56–3.49), and external material, OR 3.08 (95% CI 1.56–6.07), and more than two previous surgeries, OR 2.86 (95% CI 1.93–4.22). Diabetes mellitus showed an increased risk in the univariate analysis, OR 3.94 (95% CI 2.59–5.99), and in the group comparisons (three-fold risk). In the subgroup of diabetic foot patients, a pre-existing diabetic foot ulcer increased the risk for SSI, OR 2.99 (95% CI 1.21–7.41), compared to non-ulcered diabetic patients. In general, gram-positive cocci were the predominant pathogens in SSI. In contrast, polymicrobial infections with gram-negative bacilli were more common in contaminated foot surgeries. In the latter group, the perioperative antibiotic prophylaxis by second-generation cephalosporins did not cover 31% of future SSI pathogens. Additionally, selected groups of patients revealed differences in the microbiology of the SSI. Prospective studies are required to determine the importance of these findings for optimal perioperative antibiotic prophylactic measures.