Trends in the theory that inflammation plays a causal role in tendinopathy: a systematic review and quantitative analysis of published reviews

Abstract

Background/aimsThe contribution of inflammation to tendinopathy has been debated in the scientific literature. Several factors may contribute to this lack of clarity, including inconsistent definitions of inflammation. We hypothesised that the adoption and/or rejection of a causal link between inflammation and tendinopathy varied as a function of the ‘inflammatory component’ (eg, immune cell and molecular mediators included in published reviews).MethodsTwenty data items were collected from each review to determine conclusions about the role of inflammation in tendinopathy, specific definitions of the ‘inflammatory component,’ quality of the review and other potential correlates. Associations between correlates and a review’s conclusion about the role of inflammation in tendinopathy were tested using binomial logistic regression. The database searches retrieved 2261 unique publications: 137 fulfilled inclusion criteria after full text screenings.ResultsThere has been little support for an inflammatory component to tendinopathy until recently (2012–2015). Prior to 2012, the majority of published reviews did not discuss monocytes, macrophages or lymphocytes in tendinopathy; rather they focused on the lack of neutrophils, often referred to as ‘the inflammatory infiltrate’, or immune cells were not discussed. Reviews including monocytes and lymphocytes in their discussions were 5.23 times more likely to conclude inflammation was important than reviews that did not, p<0.001.ConclusionsData collected show growing support for an inflammatory component to tendinopathy, particularly among high-quality reviews and those that used more robust definitions of inflammation. This finding may have implications for explaining dissonance in the literature regarding a causal role for inflammation in the pathogenesis of tendinopathy.

Local Shifts in Inflammatory and Resolving Lipid Mediators in Response to Tendon Overuse

“…Inflammation occurs following either acute tendon injury (4)(5)(6)(7)(8)(9) or repetitive overuse (10)(11)(12)(13)(14)(15)(16)(17), but its role in the etiology of tendinopathy has been a matter of debate (18). The term tendinitis was classically used to describe symptoms of painful non-ruptured tendons, inferring key involvement of an inflammatory component (19).…”

“…Inflammation occurs following either acute tendon injury (4–9) or repetitive overuse (10–17), but its role in the etiology of tendinopathy has been a matter of debate (18). The term tendinitis was classically used to describe symptoms of painful non-ruptured tendons, inferring key involvement of an inflammatory component (19). However, an apparent lack of polymorphonuclear leukocytes (PMNs) within diseased tendons led to the view that tendinopathy is rather a degenerative condition of tendinosis that is devoid of inflammation (20).…”

Complement Regulation in Human Tenocytes under the Influence of Anaphylatoxin C5a

“…Tendinopathy has been defined as a chronic low grade inflammatory and degenerative musculoskeletal disease [ 1 , 2 ]. Even though the etiology of this disease is still not clearly understood, there are various hypotheses that are frequently discussed.…”

“…The collagen tears resulting from so-called micro traumata after repetitive mechanical overloading have been a long known classical explanation for the pain and functional impairment in tendinopathy [ 3 ]. Moreover, the inflammatory concept in the pathogenesis of tendinopathy has regained a wider focus [ 2 ]. A low increase in pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α is associated with the pathological tendons and the affected tenocytes [ 4 ].…”

Does glucocorticoid exposure explain the association between metabolic dysfunction and tendinopathy?

“…Earlier generations of clinicians were taught that 'tendinitis' was primarily an inflammatory condition (32), whereas contemporary research has shifted toward a 'degenerative' disease model with the key features of collagen separation, thinning, and disruption without an inflammatory cell infiltrate (33). This dichotomy between primary inflammatory versus primary degenerative is likely an oversimplification with both aspects playing a role (34,35).…”