Anatomical superficial medial collateral ligament reconstruction with posteromedial capsule reefing successfully restores valgus knee laxity.

The goal of this study was to present the results of an anatomical superficial medial collateral ligament (sMCL) reconstruction combined with reefing of the posteromedial capsule in a series of 10 patients with symptomatic valgus instability complaints in combined injuries of the knee. All patients under- went an sMCL reconstruction with reefing of the posteromedial capsule. If cruciate ligament insuf- ficiency was present, this was reconstructed as well. Pre- and postoperatively, multiple subjective knee outcome scores were obtained, and valgus stress radiographs objectively evaluated laxity. Median valgus laxity of the injured knee on valgus stress radiographs improved significantly. There was no statistically significant difference between post- operative valgus laxity of the injured knee and valgus laxity of the uninjured knee. All subjective knee outcome scores improved significantly compared with the preoperative situation. The described procedure restores valgus laxity to a level comparable to the uninjured knee.

Posterolateral corner reconstruction in combined injuries of the knee: Improved stability with Larson's fibular sling reconstruction and comparison with LaPrade anatomical reconstruction.

BACKGROUND: The goal of this prospective cohort study was to present the clinical results of a two-year follow-up of a Larson's posterolateral corner reconstruction (fibular sling) in patients with symptomatic instability of the knee. These data were compared with data of an anatomical reconstruction of the posterolateral corner as described by LaPrade et al. (combined tibial tunnel and fibular sling) [1]. METHODS: Eleven patients underwent a Larson's posterolateral corner reconstruction. Cruciate ligament ruptures were reconstructed if present. Multiple subjective knee outcome scores (VAS satisfaction score, Tegner, Lysholm, Noyes score, and IKDC subjective knee score) were obtained pre-operatively and two years after surgery. Laxity of the joint was measured using bilateral varus stress radiographs. RESULTS: All patients had concomitant ACL or PCL surgery. VAS satisfaction, the Tegner, Noyes and the IKDC subjective knee score all improved significantly. Median varus laxity of the injured knee on varus stress radiographs improved significantly from 6.2° (3.1-10.1) to 3.9° (1.1-5.7), p = .0076. Post-operative varus laxity did not return to the level of the uninjured knee: 2.7° (1-5.7), p = .028. In comparison with our data on the reconstruction technique according to LaPrade, no statistically significant differences in clinical outcome were observed. CONCLUSION: Reconstruction of the posterolateral corner in combined injuries of the knee using a Larson fibular sling technique results in improved varus stability but not to the level of the uninjured knee. Functional knee scores improved significantly. We found no differences in functional and radiological outcome between the Larson's fibular sling reconstruction and LaPrade anatomical reconstruction. LEVEL OF EVIDENCE: IV.

Medial patellofemoral ligament reconstruction for patellar maltracking following total knee arthroplasty is effective.

PURPOSE: Maltracking of the patella after total knee arthroplasty (TKA) remains a well-recognized problem. The medial patellofemoral ligament (MPFL) has shown to be important for patellar stabilization and reconstructions of the MPFL have already shown excellent functional outcomes for patellar instability of the native knee. Nevertheless, there is only limited literature on using an MPFL reconstruction for correction of patellar maltracking after TKA. In this retrospective study, a consecutive case series was evaluated. METHODS: Between 2007 and 2010, nine patients (nine knees) with anterior knee pain and symptomatic (sub)luxations of the patella after primary or revision TKA were treated by reconstruction of the MPFL in combination with a lateral release. In two cases, an additional tibial tuberosity transfer was performed, due to insufficient per-operative correction. Pre-operative work-up included a CT scan to rule out component malrotation and disorders in limb alignment. Pre- and post-operative patellar displacement and lateral patellar tilt were measured on axial radiographs. Clinical outcome was evaluated using the visual analogue scale (VAS) satisfaction, VAS pain, dislocation rate and Bartlett patella score. RESULTS: Median patellar displacement improved from 29 mm (0-44) to 0 mm (0-9) post-operatively. Median lateral patellar tilt was 45° (23-62) pre-operative and changed to a median 15° (-3 to 21) post-operative. Median VAS satisfaction was 8 (5-9) and only one patient reported a subluxing feeling afterwards. The Bartlett patella score displayed a diverse picture. CONCLUSIONS: Patellar maltracking after primary or revision TKA without malrotation can effectively be treated by MPFL reconstruction in combination with a lateral release. Only in limited cases, an additional tibial tuberosity transfer is needed. LEVEL OF EVIDENCE: IV.

Pain at the knee: the Morel-Lavallée lesion, a case series.

Post-traumatic pain at the knee is a common clinical presentation with a wide and varied differential diagnosis. The Morel-Lavallée lesion (MLL) is a rare cause of pain at the knee, caused by post-traumatic shearing of the hypodermis from the underlying fascia. The space created can fill with blood, lymph and necrotic fat giving specific findings on ultrasound and magnetic resonance (MR) evaluation. Three different cases of patients diagnosed with the MLL surrounding the knee are presented, with clinical and radiological findings. The different treatment options will be evaluated. The MLL is a rare but important cause of post-traumatic pain at the knee. Clinical exam and history are mandatory in diagnosing an MLL. Ultrasound and MR examination are very helpful in assessing the diagnosis. Various treatment options, nonsurgical as well as surgical, seem to be effective and should be considered depending on presentation and duration.

ERK-1/2 and p38 in the regulation of hypertrophic changes of normal articular cartilage chondrocytes induced by osteoarthritic subchondral osteoblasts.

OBJECTIVE: Previous studies have shown the influence of subchondral bone osteoblasts (SBOs) on phenotypical changes of articular cartilage chondrocytes (ACCs) during the development of osteoarthritis (OA). The molecular mechanisms involved during this process remain elusive, in particular, the signal transduction pathways. The aim of this study was to investigate the in vitro effects of OA SBOs on the phenotypical changes in normal ACCs and to unveil the potential involvement of MAPK signaling pathways during this process. METHODS: Normal and arthritic cartilage and bone samples were collected for isolation of ACCs and SBOs. Direct and indirect coculture models were applied to study chondrocyte hypertrophy under the influence of OA SBOs. MAPKs in the regulation of the cell-cell interactions were monitored by phosphorylated antibodies and relevant inhibitors. RESULTS: OA SBOs led to increased hypertrophic gene expression and matrix calcification in ACCs by means of both direct and indirect cell-cell interactions. In this study, we demonstrated for the first time that OA SBOs suppressed p38 phosphorylation and induced ERK-1/2 signal phosphorylation in cocultured ACCs. The ERK-1/2 pathway inhibitor PD98059 significantly attenuated the hypertrophic changes induced by conditioned medium from OA SBOs, and the p38 inhibitor SB203580 resulted in the up-regulation of hypertrophic genes in ACCs. CONCLUSION: The findings of this study suggest that the pathologic interaction of OA SBOs and ACCs is mediated via the activation of ERK-1/2 phosphorylation and deactivation of p38 phosphorylation, resulting in hypertrophic differentiation of ACCs.

Osteoarthritic cartilage chondrocytes alter subchondral bone osteoblast differentiation via MAPK signalling pathway involving ERK1/2.

Osteoarthritic subchondral bone is characterized by abnormal bone density and enhanced production of bone turnover markers, an indication of osteoblast dysfunction. Several studies have proposed that pathological changes in articular cartilage influence the subchondral bone changes, which are typical of the progression of osteoarthritis; however, direct evidence of this has yet to be reported. The aim of the present study was to investigate what effects articular cartilage cells, isolated from normal and osteoarthritic joints, may have on the subchondral bone osteoblast phenotype, and also the potential involvement of the mitogen activated protein kinase (MAPK) signalling pathway during this process. Our results suggest that chondrocytes isolated from a normal joint inhibited osteoblast differentiation, whereas chondrocytes isolated from an osteoarthritic joint enhanced osteoblast differentiation, both via a direct and indirect cell interaction mechanisms. Furthermore, the interaction of subchondral bone osteoblasts with osteoarthritic chondrocyte conditioned media appeared to significantly activate ERK1/2 phosphorylation. On the other hand, conditioned media from normal articular chondrocytes did not affect ERK1/2 phosphorylation. Inhibition of the MAPK-ERK1/2 pathways reversed the phenotype changes of subchondral bone osteoblast, which would otherwise be induced by the conditioned media from osteoarthritic chondrocytes. In conclusion, our findings provide evidence that osteoarthritic chondrocytes affect subchondral bone osteoblast metabolism via an ERK1/2 dependent pathway.