Platelet kinetics were directly analysed using intravital microscopy in the arthritic microcirculation in vivo for the first time. We provide the first evidence that platelets accumulate in arthritic vessels, indicating platelet activation due to AiA. Platelet recruitment and subsequent activation might play an important role in the pathogenesis of rheumatoid arthritis.
Autologous matrix-induced chondrogenesis (AMIC) has gained popularity in the treatment of osteochondral lesions of the talus. Previous studies have presented promising short-term results for AMIC talar osteochondral lesion repair, a 1-step technique using a collagen type I/III bilayer matrix. The aim of the present study was to investigate the mid-term effects. The 5-year results of a prospective cohort study are presented. All patients underwent an open AMIC procedure for a talar osteochondral lesion. Data analysis included general demographic data, preoperative magnetic resonance imaging findings, intraoperative details, and German version of the Foot Function Index (FFI-D) scores preoperatively and at 1 and 5 years after surgery. The primary outcome variable was the longitudinal effect of the procedure, and the influence of various variables on the outcome was tested. Of 47 consecutive patients, 21 (45%) were included. Of the 21 patients, 8 were female (38%) and 13 were male (62%), with a mean age of 37 ± 15 (range 15 to 62) years and a body mass index of 26 ± 5 (range 20 to 38) kg/m. The defect size was 1.4 ± 0.9 (range 0.2 to 4.0) cm. The FFI-D decreased significantly from preoperatively to 1 year postoperatively (56 ± 18 versus 33 ± 25; p = .003), with a further, nonsignificant decrease between the 1- and 5-year follow-up examination (33 ± 25 versus 24 ± 21; p = .457). Similar results were found for the FFI-D subscales of function and pain. The body mass index and lesion size showed a positive correlation with the preoperative FFI-D overall and subscale scores. These results showed a significant improvement in pain and function after the AMIC procedure, with a significant return to sports by the 5-year follow-up point. The greatest improvement overall was seen within the first year; however, further clinical satisfaction among the patients was noticeable after 5 years.
There is growing evidence that platelets play an important role in the development and maintenance of rheumatoid arthritis. Activation and adherence of platelets in the synovial microcirculation might be in part responsible for endothelial damage and activation of leukocytes. Recent findings show a direct influence of P-selectin on platelet- and leukocyte-endothelial cell interaction in mice with Antigen-induced Arthritis (AiA). P-selectin is only expressed by platelets and endothelial cells, not by leukocytes. Therefore, the aim of the present study was to investigate the differential influence of platelet and endothelial P-selectin on the extent of inflammation in AiA. AiA was induced in wild-type mice and in P-selectin-deficient mice from the same genetic background (four groups: each n = 7). Intravital fluorescence microscopy (IVM) was used to visualize platelets and leukocytes in the synovial microcirculation at day 8 after AiA. Platelets from either strain were fluorescence-labelled ex vivo and transferred into either strain. We were able to demonstrate a significant decrease of platelet- and leukocyte-endothelial cell interaction in P-selectin-deficient mice with AiA in comparison to wild-type mice with AiA. When wild-type platelets were donated into P-selectin-deficient AiA recipients, the leukocyte-endothelial cell interaction was significantly increased compared to the group consisting of P-selectin-deficient recipient and donor mice. These are the first in vivo results showing that the P-selectin stored in platelets is at least partly responsible for the leukocyte-endothelial cell interaction and the resulting tissue damage in AiA. In the future, a suppression of platelet P-selectin could potentially become a treatment option for reducing the effects of rheumatoid arthritis.
We have demonstrated for the first time in vivo a significant decrease in the interaction of platelets and leucocytes with the endothelium in P-selectin-deficient mice with AiA and a reduction in clinical and histological symptoms of arthritis. These findings suggest that leucocyte-endothelial cell interactions depend at least partially on platelet P-selectin and therefore platelets may be responsible for the leucocyte tissue damage in AiA.
Purpose
The purpose of this study was to compare patients with osteochondral lesions of the talus (OCLT) with and without concomitant chronic ankle instability (CAI).
Methods
Data from the German Cartilage Registry (KnorpelRegister DGOU) for 63 patients with a solitary OCLT were used. All patients received autologous matrix‐induced chondrogenesis (AMIC) for OCLT treatment. Patients in group A received an additional ankle stabilisation, while patients in group B received AMIC alone. Both groups were compared according to demographic, lesion‐related, and therapy‐related factors as well as baseline clinical outcome scores at the time of surgery. The Foot and Ankle Ability Measure (FAAM), the Foot and Ankle Outcome Score (FAOS), and the Numeric Rating Scale for Pain (NRS) were used.
Results
Patients in group A were older compared to group B [median 34 years (range 20–65 years) vs. 28.5 years (range 18–72 years)]; the rate of trauma‐associated OCLTs was higher (89.7% vs. 38.3%); more patients in group A had a previous non‐surgical treatment (74.1% vs. 41.4%); and their OCLT lesion size was smaller [median 100 mm2 (range 15–600 mm2) vs. 150 mm2 (range 25–448 mm2)]. Most OCLTs were located medially in the coronary plane and centrally in the sagittal plane in both groups. Patients in group A had worse scores on the FAOS quality‐of‐life subscale compared to patients in group B.
Conclusion
Patients with OCLT with concomitant CAI differ from those without concomitant CAI according to demographic and lesion‐related factors. The additional presence of CAI worsens the quality of life of patients with OCLT. Patients with OCLT should be examined for concomitant CAI, so that if CAI is present, it can be integrated into the treatment concept.
Level of evidence
IV.
The method is very effective to treat even severe deformities with or without metatarsalgia. The amount of correction is similar to open procedures. We recommend cadaver training to become familiar with this technique. Thus, complications such as nerve, vessel or tendon injuries can be avoided. The intraoperative radiation exposure remains significantly elevated even for experienced surgeons. In addition to the aesthetic benefits, there is less soft tissue traumatization compared to conventional open procedures. There is no need of bloodlessness. The minimally invasive Chevron and Akin osteotomy is a safe and powerful technique for the treatment of hallux valgus deformity.
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