Exploring the role of intratendinous pressure in the pathogenesis of tendon pathology: a narrative review and conceptual framework

Abstract

Despite the high prevalence of tendon pathology in athletes, the underlying pathogenesis is still poorly understood. Various aetiological theories have been presented and rejected in the past, but the tendon cell response model still holds true. This model describes how the tendon cell is the key regulator of the extracellular matrix and how pathology is induced by a failed adaptation to a disturbance of tissue homeostasis. Such failure has been attributed to various kinds of stressors (eg, mechanical, thermal and ischaemic), but crucial elements seem to be missing to fully understand the pathogenesis. Importantly, a disturbance of tissue pressure homeostasis has not yet been considered a possible factor, despite it being associated with numerous pathologies. Therefore, we conducted an extensive narrative literature review on the possible role of intratendinous pressure in the pathogenesis of tendon pathology. This review explores the current understanding of pressure dynamics and the role of tissue pressure in the pathogenesis of other disorders with structural similarities to tendons. By bridging these insights with known structural changes that occur in tendon pathology, a conceptual model was constituted. This model provides an overview of the possible mechanism of how an increase in intratendinous pressure might be involved in the development and progression of tendon pathology and contribute to tendon pain. In addition, some therapies that could reduce intratendinous pressure and accelerate tendon healing are proposed. Further experimental research is encouraged to investigate our hypotheses and to initiate debate on the relevance of intratendinous pressure in tendon pathology.

Keywords: Tendinopathy; Tendinosis; Tendon.

Figure 1

Conceptual framework describing the role of intratendinous pressure in the pathogenesis of tendon pathology. CS, chondroitin sulfate; DS, dermatan sulfate; HA, hyaluronan.

Figure 2

Illustration of the enthesis showing the presence of fibrocartilage in areas where tendon and bone are adjacent. Picture adapted with permission from Elsevier.

Figure 3

Illustration of how swelling pressure in tendon pathology may occur, resulting in an increased intratendinous resting pressure.

Figure 4

Illustration of how ischaemia may occur in tendons due to an increased IRP. (A) Normal fascicle in which pressure gradient is necessary for adequate intrafascicular circulation. (B) IRP in tendon pathology may be increased, inducing vascular collapse and a reduced arteriovenous pressure gradient. The resulting hypoxia stimulates vascular permeability and the formation of leaky neovessels, which further contribute to an increase in IFP. It should be noted that the IRP can also increase interfascicularly with the same phenomena, but with the epitenon as the main barrier sheath. IFP, interstitial fluid pressure; IRP, intratendinous resting pressure.

Figure 5

Illustration of how IDP occurs in tendons, resulting in fluid exudation. (A) During tensile loading, tendon fluid moves radially from the tendon core to the outside, due to lateral contraction and the associated increase in pressure. (B) In tendon pathology, hydraulic permeability decreases due to the accumulation of GAGs and PGs, resulting in fluid entrapment and higher IDP. GAGs, glycosaminoglycans; IDP, intratendinous dynamic pressure; PGs, proteoglycans.

Figure 6

Illustration of how disruption of the interfascicular matrix may occur in tendons due to high intratendinous dynamic pressure.

Figure 7

Illustration demonstrating the importance of the location of fluid accumulation.