Update on contribution of hip labral tears to hip pain: A narrative review.

Hip labral tears are found in 22-55% of individuals with hip pain, but labral tears without cysts are usually not responsible for hip pain, which originates mostly from other structures than the torn labrum, like osteochondral, but also tendinous injuries (rectus femoris, gluteus minimus, iliopsoas) or capsulo-ligamentous tears (iliofemoral ligaments, ligament teres). Those lesions are mainly the consequences of underlying unrecognized functional acetabular dysplasia, and/or femoroacetabular impingements. Although the early repair of labral tears in young sportsmen induces a marked and lasting relief, and might delay the onset of osteoarthritis, the microinstability fostered by labral damages seems less important than underlying dysplasias/impingements. This narrative review details recent findings on: (i) the various mechanisms of pain associated with labral tears; (ii) few evidence for hip microinstability induced by isolated labral tears; (iii) how to best detect labral tears, both clinically (including through IROP test) and on imaging (MRI, MRA, computed tomography arthrography, ultrasound). Some authors suggested to use pull-out tests during surgery, but pulling of hips do not seem to increase much diagnostic performances of ultrasounds. Ultrasound-guided intra-articular and peri-articular injections may tell how often hip pain is exclusively induced by peri-capsular injuries secondary to the acetabular dysplasia/femoro-acetabular impingements already responsible for labral tears. Further works could tell whether labral repair, tendinous debridement, plication of capsule, and/or focal denervation, may induce lasting reliefs of pain induced by the chronic contraction of surrounding muscles (rectus femoris, gluteus minimus, psoas), whose deep aponeuroses mix with the superficial fibres of the thick hip capsule.

Prolonged response on olaparib maintenance in metastatic pancreatic acinar cell carcinoma associated with a germline BRCA 2 mutation, revealed by severe panniculitis.

This 38-year-old man has a familial BRCA2 mutation. He presented with skin erythema, polyarthritis, dactylitis, and febrile erythema nodosum; a biopsy of a liver metastase revealed acinar cell carcinoma of the pancreas. After FOLFIRINOX, olaparib was initiated, and 24 months after, the patient was PS 0 and asymptomatic.

Inadequacies of the Lasègue test, and how the Slump and Bowstring tests are useful for the diagnosis of sciatica.

Diagnosis of sciatica mainly relies on pain reproduction by stretching of the lumbar roots since neurological examination and medical history are usually not sufficient to guarantee diagnosis. The Lasègue test is the most popular method, which starts with the straight leg-raising test (SLR). However it is not perfect, and is not always well performed or interpreted. Passive ankle dorsiflexion at the end of the SLR (Bragard test) is more sensitive, but can also remain normal in some cases of sciatica. Other stretching tests can help to recognise lumbar root damage in patients with poorly defined pain in a lower extremity: firstly, the Christodoulides test, i.e. reproduction of L5 sciatic pain by a femoral stretch test; secondly, the Slump test, performed on a patient in a sitting position, by slowly extending their painful leg then passively bending their neck (or the opposite); and thirdly, the Bowstring test, which requires, at the end of the Lasègue test, once the knee has been slightly flexed, pressing on the course of the peroneal and/or tibial nerves in the popliteal fossea to try and reproduce the exact pain felt by the patient. The combination of all these tests takes less than 2minutes, and could improve both the sensitivity and specificity of the physical examination for the diagnosis of sciatica. This article is a review of the limitations of the Lasègue/SLR tests and of the efficacy of these other tests for stretching the lumbar roots.

Enhanced BMP-2/BMP-4 ratio in patients with peripheral spondyloarthritis and in cytokine- and stretch-stimulated mouse chondrocytes.

BACKGROUND: Excessive bone formation in the entheses is one of the features of peripheral spondyloarthritis (SpA). Complex pathological mechanisms connecting inflammation, mechanical stress, and ossification are probably involved. We focused on bone morphogenetic protein (BMP)-2, -4, and -7 as possible mediators of this process. METHODS: BMP-2, -4, and -7 concentration was measured by ELISA in synovial fluids (SFs) of SpA (n = 56) and osteoarthritic (n = 21) patients. Mouse organotypic ankle cultures were challenged by a pro-inflammatory cocktail. Mouse primary chondrocytes, osteoblasts, or tenocytes were treated with TNF-α, interleukin (IL)-17, or IL-22 and/or subjected to cyclic stretch, or with recombinant BMP-2 or -4. RESULTS: In SpA SFs, if BMP-7 was barely detectable, BMP-2 concentration was higher and BMP-4 was lower than in osteoarthritic samples, so that BMP-2/BMP-4 ratio augmented 6.5 folds (p < 0.001). In SpA patients, TNF-α, IL-6, and IL-17 levels correlated this ratio (n = 21). Bmp-2/Bmp-4 ratio was similarly enhanced by cytokine treatment in explant and cell cultures, at mRNA level. In particular, simultaneous application of TNF-α and cyclical stretch induced a 30-fold increase of the Bmp-2/Bmp-4 ratio in chondrocytes (p = 0.027). Blockade of prostaglandin E2 and IL-6 production had almost no effect on the stretch-induced regulation of Bmp-2 or -4. Osteoinductive effects of BMP-4, and to a lesser extend BMP-2, were identified on cultured chondrocytes and tenocytes. CONCLUSIONS: Our results first settle that BMP factors are locally deregulated in the SpA joint. An unexpected decrease in BMP-4 could be associated to an increase in BMP-2, possibly in response to mechanical and/or cytokine stimulations.

Rotator Cuff Tenocytes Differentiate into Hypertrophic Chondrocyte-Like Cells to Produce Calcium Deposits in an Alkaline Phosphatase-Dependent Manner.

Calcific tendonitis is a frequent cause of chronic shoulder pain. Its cause is currently poorly known. The objectives of this study were to better characterize the cells and mechanisms involved in depositing apatite crystals in human tendons. Histologic sections of cadaveric calcified tendons were analyzed, and human calcific deposits from patients undergoing lavage of their calcification were obtained to perform infrared spectroscopy and mass spectrometry-based proteomic characterizations. In vitro, the mineralization ability of human rotator cuff cells from osteoarthritis donors was assessed by alizarin red or Von Kossa staining. Calcifications were amorphous areas surrounded by a fibrocartilaginous metaplasia containing hypertrophic chondrocyte-like cells that expressed tissue non-specific alkaline phosphatase (TNAP) and ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), which are two key enzymes of the mineralization process. Calcific deposits were composed of apatite crystals associated with proteins involved in bone and cartilage development and endochondral bone growth. In vitro, tenocyte-like cells extracted from the rotator cuff were able to mineralize in osteogenic cultures, and expressed TNAP, type X COLLAGEN, and MMP13, which are hypertrophic chondrocytes markers. The use of a TNAP inhibitor significantly prevented mineral deposits. We provide evidence that tenocytes have a propensity to differentiate into hypertrophic chondrocyte-like cells to produce TNAP-dependent calcium deposits. We believe that these results may pave the way to identifying regulating factors that might represent valuable targets in calcific tendonitis.