Background Injury of the tarsometatarsal (TMT) joint complex, known as Lisfranc injury, covers a wide range of injuries from subtle ligamentous injuries to severely displaced crush injuries. Although it is known that these injuries are commonly missed, the literature on the accuracy of the diagnostics is limited. The diagnostic accuracy of non-weight-bearing radiography (inter-or intraobserver reliability), however, has not previously been assessed among patients with Lisfranc injury. Methods One hundred sets of foot radiographs acquired due to acute foot injury were collected and anonymised. The diagnosis of these patients was confirmed with a CT scan. In one-third of the radiographs, there was no Lisfranc injury; in onethird, a nondisplaced (< 2 mm) injury; and in one-third, a displaced injury. The radiographs were assessed independently by three senior orthopaedic surgeons and three orthopaedic surgery residents. Results Fleiss kappa (κ) coefficient for interobserver reliability resulted in moderate correlation κ = 0.50 (95% CI: 0.45-0.55) (first evaluation) and κ = 0.58 (95% CI: 0.52-0.63) (second evaluation). After three months, the evaluation was repeated and the Cohen's kappa (κ) coefficient for intraobserver reliability showed substantial correlation κ = 0.71 (from 0.64 to 0.85). The mean (range) sensitivity was 76.1% (60.6-92.4) and specificity was 85.3% (52.9-100). The sensitivity of subtle injuries was lower than severe injuries (65.4% vs 87.1% p = 0.003). Conclusions Diagnosis of Lisfranc injury based on non-weight-bearing radiographs has moderate agreement between observers and substantial agreement between the same observer in different moments. A substantial number (24%) of injuries are missed if only non-weight-bearing radiographs are used. Nondisplaced injuries were more commonly missed than displaced injuries, and therefore, special caution should be used when the clinical signs are subtle. Level of evidence III.

The local immunoreactivity of C-reactive protein (CRP) was studied in a heterotopic porcine model of posttranplant obliterative bronchiolitis (OB). Bronchial allografts and control autografts were examined serially 2–28 days after subcutaneous transplantation. The autografts stayed patent. In the allografts, proliferation of inflammatory cells (P < .0001) and fibroblasts (P = .02) resulted in occlusion of the bronchial lumens (P < .01). Influx of CD4+ (P < .001) and CD8+ (P < .0001) cells demonstrated allograft immune response. CRP positivity simultaneously increased in the bronchial walls (P < .01), in macrophages, myofibroblasts, and endothelial cells. Local CRP was predictive of features characteristic of OB (R = 0.456–0.879, P < .05−P < .0001). Early obliterative lesions also showed CRP positivity, but not mature, collagen-rich obliterative plugs (P < .05). During OB development, CRP is localized in inflammatory cells, myofibroblasts and endothelial cells probably as a part of the local inflammatory response.

Epithelial cell injury, inflammation, progressive fibrosis, and airway obliteration are histological features of post-transplant obliterative bronchiolitis (OB). Cyclooxygenase (COX)-2 is expressed in acute and chronic inflammatory responses. Our aim was to elucidate the possible role of COX-2 in post-transplant OB by using a heterotopic bronchial porcine model. Bronchial allografts from non-related donors were transplanted subcutaneously into 24 random-bred domestic pigs, each weighing about 20 kg. Groups studied had grafts, non-treated allografts, allografts given cyclosporine A (CsA), methylprednisolone (MP), and azathioprine (Aza), and allografts given CsA, MP, and everolimus. Grafts were serially harvested during a follow-up period of 21 days for histology (H&E) and immunohistochemistry. Immunostaining was performed with monoclonal IgG against human COX-2 peptide, and histological alterations and immunohistochemical positivity were graded on a scale from 0 to 5. Epithelial COX-2 index was calculated by multiplying the percentage of positive cells by grade of epithelial COX-2 intensity. Ischaemic epithelial loss, evident in all implants, recovered rapidly in autografts, and bronchi remained patent. Epithelial loss in non-treated allografts preceded fibroblast proliferation, resulting in total luminal obliteration. In CsA-, MP-, and Aza-treated allografts epithelial destruction and luminal obliteration were delayed, and these were prevented in CsA-, MP-, and everolimus-treated allografts. COX-2 expression due to operative ischaemia was evident in all implants on day 2. Thereafter, the epithelial COX-2 index preceded epithelial injury and obliteration. During the inflammatory response and fibroblast proliferation, COX-2 expression occurred in macrophages and fibroblasts. In conclusion, in the early stage of OB development, COX-2 induction occurred in airway epithelial cells prior to luminal obliteration. In addition, the observation that COX-2 expression in macrophages and fibroblasts paralleled the onset of inflammation and fibroblast proliferation indicates a role in OB development, but the causal relationships need further study.

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