Prior to the 1990s pain arising from tendons was referred to as tendinitis, implying that inflammation was responsible for the pathological process. This view was both widely accepted and deeply ingrained in the medical literature. 1 Treatment strategies at this time were largely anti-inflammatory in nature and relied heavily on non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroids. 2 , 3

The move away from ‘tendinitis’ thinking was summed up concisely in a BMJ Editorial by Khan et al 1 when practitioners and educators were urged “to accept the irrefutable evidence that the term tendinitis must be abandoned to highlight a new perspective on tendon disorders”. At the time of the Editorial it was necessary for a strong message to be sent that chronic tendinopathy had a different aetiology to inflammatory conditions such as RA, and to emphasise that traditional strategies such as corticosteroid injection and NSAIDs do not adequately address the pathology. Although this remains an important message, we believe to regard all chronic tendinopathy as entirely non-inflammatory is an oversimplification to the point of being misleading.

Initially recognised by Puddu et al 4 as long ago as the 1970s, in chronic tendinopathy there is an absence of acute inflammatory cells in the load-bearing regions of tendons. 4 As histological data became more readily available this view became increasingly recognised. Several studies demonstrated collagen separation, thinning and disruption without an inflammatory cell infiltrate. 5–7 There was also evidence from some animal studies that degenerative non-inflammatory tendon changes could be experimentally introduced over a brief (1 or 2 week) period. 8 The pathology of chronic tendon disorders was correctly recognised as being very different from that of a characteristically inflammatory disease, such as rheumatoid arthritis (RA).

Degeneration without inflammation: the paradigm of the 2000s

During the first decade of the 21st century ‘non-inflammatory’ or ‘degenerative’ theories have dominated thinking in tendinopathy. Various models have been proposed. First there are models that attempt to explain why tendons fail. The cumulative damage and vascular insufficiency models fall into the first group.2 Second, a group of models attempts to explain why tendons fail to repair themselves and includes the ‘failed healing response’9 and the continuum theories of tendinopathy.10 These theories and the degenerative ‘paradigm’ in general, have become extremely influential.

These ‘degenerative’ models have led to attempts to improve treatment and rehabilitation of the failing tendon. The common treatments that have been adopted during the 1990s can be broadly classified in four groups:

Physical exercises including eccentric exercises (EE) or other progressive loading regimes. Treatments using blood and blood products that aim to improve tendon healing and remodelling. Treatments that aim to reduce the pain associated with tendinopathy rather than heal the tendon itself (such as sclerosant or high-volume injections). Extracorporeal shock wave therapy (ESWT).

While there may be a degree of overlap between the treatment groups (eg, ESWT may influence pain processing) the point is none of these treatments are anti-inflammatory in nature.

Certainly much emphasis over the last 10 years has been placed on physical therapies. Eccentric exercises are shown to be effective in managing mid-portion Achilles tendinopathy.11 However, in subsequent studies the very high success rate found in this paper have not been repeated, highlighting the difficulties of EE in less-athletic populations.12 Furthermore, the success of this technique has not been satisfactorily demonstrated for other tendons.13–15 Other rehabilitation models that incorporate a variety of exercises, gradually increasing both load and velocity as the patient's tolerance improves, have also been explored.16 ,17

A second area of treatment options are blood and blood products, including bone marrow-derived cells. Initial encouraging data from the equine field demonstrated the potential of stem cells to repair the hypoechoic lesions seen on ultrasound (US).18 This method, requiring a bone marrow biopsy and in vitro cell expansion, is complicated and has not become routine in human clinical practice.

However, in humans, many attempts have been made to help ‘repair’ tendons by the use of more readily available agents particularly autologous blood and autologous blood products (principally platelet-rich plasma, PRP). The suggestion is that the cells and growth factors (such as vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF-1) in PRP)19 or other components of these preparations promote healing. While small uncontrolled studies have shown benefits from these treatments,20 ,21 evidence of the efficacy of these treatment strategies in good-quality in vivo studies is currently lacking. Indeed for PRP the level 1 evidence is that PRP is ineffective for mid-portion Achilles tendinopathy.22 Proponents of PRP argue that as there are numerous ways of preparing PRP and some methods may be more effective than others. Nevertheless, there is currently minimal scientific evidence that either PRP or autologous blood is effective when compared to placebo or no injection and further studies are going on.

The limitations of physical therapies and blood product injections in healing tendons have led to a different approach—with the aim of controlling pain through the disruption of the neural ingrowth that often accompanies neovessel formation in chronic tendinopathy.23 We describe these techniques as denervation procedures. Techniques in this emerging area include sclerosant therapy (eg, polidocanol and possibly dextrose),24 high-volume/tendon stripping injections25 and some surgical techniques (such as paratenon stripping). These techniques are likely to exert their beneficial effect by interruption of neural ingrowth. As shock waves are toxic to peripheral nerves it is possible that ESWT may derive a beneficial effect, at least in part, from a direct effect on peripheral nerves.26

Throughout the last decade the belief that chronic tendon conditions occur due to degeneration has become the prevailing paradigm. Unfortunately, with the possible exception of mid-Achilles tendinopathy, the last decade has not provided us with therapies that are successful at ‘healing’ the failing tendon.

However, is it certain that inflammation is not involved in the development or progression of tendinopathy? And if so are there other potential treatment options that have been overlooked?