Timing of postoperative weightbearing in the treatment of traumatic chondral injuries of the knee in athletes - A systematic review of current concepts in clinical practice.

BACKGROUND: Surgery aims to stimulate healing and enable a safe return to sport in athletes with symptomatic cartilage lesions of the knee. Timing of postoperative weightbearing is crucial, balancing a stimulation of the healing and avoiding reinjury.To explore current concepts of timing to partial and full weightbearing and rate of return to sport in athletes after articular cartilage surgery of the knee.Systematic Review of studies with level of evidence I-III. METHODS: Four databases (Pubmed, Web of Science, Scopus and Embase) were searched using a predetermined keyword strategy. Two independent reviewers screened results according to inclusion and exclusion criteria. Modified Coleman Methodology Score (mCMS) was used for the quality assessment. RESULTS: 5294 records were found. Data from ten studies was extracted after duplicate removal, title and abstract screening and full-text evaluation. Eight of the ten studies included a detailed rehabilitation protocol, including 336 out of a total athletic population of 401. 62% began partial weightbearing (PWB) 1-2 weeks postoperatively, while 38% began within 3-4 weeks. The studies that had a later PWB all returned to full weightbearing (FWB) within 6-8 weeks. One study with early PWB returned to early FWB, while the other two returned 10-12 weeks postoperatively. "Return to Sport" (RTS) was the most common reported outcome measure, with most studies reporting RTS at 80% or higher. CONCLUSION: There is no clear evidence that the timing of weightbearing (WB) affects the outcome and return to sport in athletes after surgery for focal full-thickness cartilage lesions of the knee. On the other hand, there seems to be no adverse effects in adopting an early WB strategy, currently defined differently by different authors. Further studies directly comparing the timing of WB for specific surgical procedures in athletes and with relevant control groups is recommended. There is a need for a consensus in regard to more exactly defining "early" vs "late" weightbearing in relation to a universal and precisely defined state of healing.

Are muscle weakness and stiffness risk factors of the development of rotator cuff tendinopathy in overhead athletes: a systematic review.

BACKGROUND: Underlying muscle weakness and stiffness may increase the risk of developing rotator cuff tendinopathy. This systematic review aims to assess existing prospective studies to summarize whether muscle weakness and stiffness are risk factors for the development of rotator cuff tendinopathy in overhead athletes. METHODS: A systematic search was performed using PRISMA guidelines. Prospective studies measuring muscle strength or stiffness and the incidence of rotator cuff tendinopathy were included. Quality assessment was performed with the Newcastle-Ottawa quality assessment scale. RESULTS: The search yielded six studies, with a total of 523 trained overhead athletes followed up for one season. External rotation (ER) and internal rotation (IR) strength were described as protective factors against the development of rotator cuff tendinopathy. Athletes who did not sustain shoulder injuries had statistically stronger eccentric IR (p < 0.01) and ER (p < 0.05) strength in the pre-season assessment. Muscle stiffness indicated by limited range of motion of <106° for shoulder ER was described as a risk factor with an odds ratio of 1.12 (p < 0.001). Imbalance between ER and IR strength was reported as risk factors for shoulder injuries in two studies, with a relative risk of 2.57 (p < 0.05) reported in one study. Supraspinatus weakness was also reported as a risk factor for shoulder injuries in one study. CONCLUSION: Limited evidence support ER, IR weakness, limited ER range of motion, and very limited evidence support imbalance in ER/IR strength, and supraspinatus weakness as risk factors for rotator cuff tendinopathy in overhead athletes. No existing studies investigated the general population on this topic. Future cohort studies may improve on existing evidence with investigations on the general public, a longer follow-up time, clearly documented injury history, and a stringent diagnosis to rotator cuff tendinopathy.

A systematic review of inflammatory cells and markers in human tendinopathy.

BACKGROUND: This article systematically reviews the current evidence regarding inflammation in Tendinopathy with the aim to increase understanding of a potential common pathophysiology. METHODS: Following the PRISMA statements, the terms: (tendinopathy OR (tendons AND rupture)) AND (inflammation OR (inflammation AND cells) OR immune system OR inflammation mediators OR bacteria) were used. One thousand four hundred thirty-one articles were identified which was screened down to 53. RESULTS: 39/53 studies mentioned inflammatory cells but had contradicting conclusions. Macrophages were the most common cell type and inflammatory markers were detectable in all the articles which measure them. CONCLUSIONS: The included studies show different conclusions, but this heterogeneity is not unexpected since the clinical criteria of 'tendinopathy' encompass a huge clinical spectrum. Different 'tendinopathy' conditions may have different pathophysiology, and even the same clinical condition may be at different disease stages during sampling, which can alter the histological and biochemical picture. Control specimen sampling was suboptimal since the healthy areas of the pathological-tendon may actually be sub-clinically diseased, as could the contralateral tendon in the same subject. Detection of inflammatory cells is most sensitive using immunohistochemistry targeting the cluster of differentiation markers, especially when compared to the conventional haematoxylin and eosin staining methods. The identified inflammatory cell types favour a chronic inflammatory process; which suggests a persistent stimulus. This means NSAID and glucocorticoids may be useful since they suppress inflammation, but it is noted that they may hinder tendon healing and cause long term problems. This systematic review demonstrates a diversity of data and conclusions in regard to inflammation as part of the pathogenesis of Tendinopathy, ranging from ongoing or chronic inflammation to non-inflammatory degeneration and chronic infection. Whilst various inflammatory markers are present in two thirds of the reviewed articles, the heterogenicity of data and lack of comparable studies means we cannot conclude a common pathophysiology from this systematic review.

A high glucose level stimulate inflammation and weaken pro-resolving response in tendon cells - A possible factor contributing to tendinopathy in diabetic patients.

BACKGROUND: Tendinopathy is a chronic disorder that affects a huge population, and is causing high socioeconomical impacts worldwide. Tendinopathy was reported to be more prevalent in diabetic patients, and chronic inflammation was proposed to play an important role in its development. It was also known that diabetic patients present in a pro-inflammatory state. There is a possibility that the high glucose environment in diabetic patients lead to chronic inflammation in the tendon, and eventually the development of tendinopathy. In this study, we would simulate the diabetic environment in an in vitro setup, to assess the effect of a high glucose level on cultured tendinopathic and healthy tendon derived stem cells (TDSCs) under inflammatory stress. We would first like to assess whether there are differences between the inflammatory response in tendinopathic and healthy TDSCs. We would then investigate whether a high glucose level may lead to changes in the inflammatory response in healthy tendon cells. METHODS: Tendinopathic TDSCs were cultured from 2 torn rotator cuff tendons and 1 ruptured patellar tendon. Healthy TDSCs were cultured from 3 gender matched healthy hamstring tendons. Cells were stimulated by either 2ng/ml IL-1B for 24 hours, 11.1 mmol/L glucose for 24 hours, or both. mRNA was collected and processed for qPCR targeting B-actin, ALOX12, ALOX15, FPR1, FPR2, ChemR23, and COX2. RESULTS: Upregulation of FPR1 (p=0.050) ChemR23 (p=0.050), ALOX15 (p=0.050) was significantly weakened when comparing tendinopathic and healthy TDSCs stimulated with IL-1b. The upregulation of ALOX15 (p=0.050), was significantly lower in stimulated healthy TDSCs in a high glucose environment when comparing with those stimulated under a regular glucose level. A high glucose level also induced upregulation of COX2 (p=0.046) in healthy TDSCs and tendinopathic TDSCs (p=0.050). CONCLUSION: The results of this study provide a possible explanation to the increased risk to develop tendinopathy in diabetic patients. Chronic inflammation observed in tendinopathy may be due to the weakening of pro-resolving responses in tendinopathic TDSCs, and a high glucose environment may lead to chronic inflammation and ultimately tendinopathy by persistent stimulation and weakening of pro-resolving response in healthy TDSCs.