Tendons & Tendinopathies (1/2)


Tendons are a specialized fibrous connective tissue that connects muscle to bones. Tendons are composed of densely packed bundles of collagen fibers, which are arranged in parallel bundles and wrapped in a protective sheath of connective tissue. They transmit the force of muscle contraction to the bones, allowing movement to occur. The Musculotendinous junction is the location where the tendon meets the muscle and functions to dissipate force generated by muscle contraction and to ensure that the muscle and tendon fibers are properly aligned for efficient movement. (Sharma, P et al 2006) The osteotendinous junction is the location in which the tendon meets the bone, and this mineralized structure functions to decrease collagen fibers from bending, fraying, shearing, and failing. (Sharma, P et al 2006)

They contain tenocytes, which are fibroblast-like cells that are important for maintaining the microenvironment of tendons, production of collagen (constitutes 65-80% of dry mass of tendon) and synthesizing extracellular matrix. (Xu Y et al, 2008) (Screen, HR 2015) (Heinemeier, K et al 2013) This composition allows for load absorption and force transmission from muscle to bones, making it essential in movement. It facilitates forces at the joints, creates explosively and contributes to stability during locomotive states. (Bohm et al, 2015) (Xu Y et al, 2008) (Ahmad, Z et al 2019) More importantly, they adapt. Adaptations occur over time in response to the demands stressed upon the tissues or the lack thereof. (Docking, S et al 2019) Loads can induce positive adaptations to mechanical stimuli; however, tendons are mechanoresponsive, making it paradoxical. Excessive mechanical loads are considered to be an important contributor in the etiology of tendinopathy. (Bohm et al, 2015) (Docking, S et al 2019)

Load capacity in tendons is the ability to perform movements while maintaining the volume and frequency required, without exacerbating symptoms. (Docking, S et al 2019) The foundation of tendon load capacity begins in early childhood and the core of the tendon primarily matures around puberty (~ 17 YO). The rate of tissue renewal typically stabilizes thereafter. (Heinemeier, K et al 2013) However, the components around the core of the tendon can be manipulated such as collagen orientation, tendon size (atrophy or hypertrophy), and chemical production (i.e collagen). Additionally, there are other variables that influence the magnitude of load capacity including: frequency, loading rate, joint angles, load duration and dynamic vs. static loading. (Bohm et al, 2015) (Arampatzis A, et al 2010).


(Screen, H. R. et al, 2015)




Keynote Definitions


degeneration of a tendon in the absence of intratendinous inflammation. Often characterized by necrosis, calcification and neovascularization. (Maffuli, n et al 1998) (Ahmad, Z et al 2019)


acute edema and hyperemia associated with inflammatory cells, likely due to a movement friction. (i.e. DeQuervain tenosynovitis) (Maffuli, n et al 1998) (Ahmad, Z et al 2019)



depicts a state of inflammation occurring in the tendon. It refers to a clinical syndrome, not the histopathological entity. More recent data suggests this is an inaccurate delineation, due to the conflicting studies regarding the existence of inflammatory cells in tendons, thus abandoning this term clinically. (Ahmad, Z et al 2019) (Maffuli, n et al 1998)


a clinical diagnosis, characterized by changes within the tendon typically coupled with pain, reduced tendon mechanics and reduced load tolerance – not linked to an underlying structural abnormality.  (Screen, HRC et al 2016) (Silbernagel et al, 2020) (Ahmad, Z et al 2019)



A Tendinopathy is a clinical diagnosis, characterized by changes within the tendon typically coupled with pain, reduced tendon mechanics and reduced load tolerance – not linked to an underlying structural abnormality.  (Screen, HRC et al 2016) (Silbernagel et al, 2020) (Ahmad, Z et al 2019) Tendons can be further characterized by the site of symptoms, insertional tendinopathy, midportion tendinopathy and proximal musculotendinous junction tendinopathies. As previously mentioned, tendons are mechanoresponsive; thus, tendinopathies often result from loading the tissues beyond their adaptive capacity with inadequate recovery over a period of time. (Bohm et al, 2015) Tendinopathies can occur in any tendon and region of the tendon (insertional, mid-portion or musculotendinous junction). They are often near the insertion or enthesis; typically, where increased stress loads occur. (Bohm et al, 2015) Tendon pathology can afflict many joints, including shoulders, elbows, hands, knees and ankles. They can be seen amongst various populations; however, it has been predominately seen in adult male athletes. (Silbernagel et al, 2020). The pathoetiology of tendinopathies is multifactorial in nature and complex. There are some notable intrinsic (systemic and biomechanical) and extrinsic contributing factors to the etiology of tendinopathy, but no single causation. Some risk factors found in literature regarding tendinopathies include metabolic/endocrine conditions (diabetes, hypothyroidism, hyper/hypoparathyroidism, etc), rheumatological conditions (RA, DISH, etc) and a few medications (Fluoroquinolone, glucocorticoids, retinoids), but are still underway in observational studies. (Cardoso TB, 2019) Some histopathologic changes have been commonly seen in tendinopathies, such as disorganized and/or denatured collagen bundles, hypoxia, lipid vacuoles and apoptosis. (Xu Y et al, 2008) Structurally, changes in the tendon result in increased cross-sectional areas and overall reduced stiffness. Stiffness has been a continuous finding in tissue vigor, determined by collagen content and orientation. In some pathological tendons, it notably declines and aggregates. (Magnusson, P et al 2019) (Arya & Kulig, 2010). However, it isn’t uncommon to see normal images in pathological tendons, and vice versa; as images have shown many inconsistencies and don’t often corroborate clinical symptoms (Ahmad, Z et al 2019). On a cellular level, some individuals with tendinopathies have microscopic changes within the tissue structure, such as cell degradation and apoptosis. This includes an increase in thickness (tendinosis), a loss of collagen, hypervascularization, and an overproduction of proteoglycans, which has been perceived as inflammation due to its visual presentation (i.e. swelling, soreness). (Silbernagel et al, 2020) Data suggests that an acute rise in inflammatory mediators (i.e. exercise) is important for collagen turnover and for tendon adaption. (Magnusson, P et al 2019) However, the tendinopathic association to inflammation is still debated due to the inconsistent studies. Recent studies reveal the presence of inflammatory markers or inflammatory cells; however, it is unclear if their role is in adaptive tissue remodeling, systemic inflammation or due to acute insults. (Jomaa, G. et al 2020). Inflammation is not typically seen in chronic tendinopathies. In fact, biopsies have shown an absence of inflammatory cell infiltration in tendons. (Longo, UG et al 2008) (Longo, UG et al 2007) (Magnusson, P et al 2019). Thus, nullifying the term “tendinitis” (‘itis’ = inflammation) and using tendinopathy as an umbrella term for changes seen within the tendon. The importance of this distinction lies within the efficacy of treatment. When treating inflammation, common therapies such as over the counter NSAIDs (non-steroidal anti-inflammatory drugs) or corticosteroids are typically used, but this could be detrimental in tendons, making it critical to understand these biochemical changes. (Docking, S et al, 2019) (Silbernagel et al, 2020) What may seem like an acute flare up, is actually a progressive failure of a chronic healing response. With so much variability and inconsistency, the effectiveness of any drug management is currently controversial at best when treating tendinopathies. (Longo, UG et al 2018). Thus, it would be practical to shift efforts into investigating other forms of conservative management. A comprehensive patient history will best reveal individualistic contributing factors, subsequently piloting appropriate treatment options for subjective pain relief.


Table 1 Factors implication in chronic tendinopathy 

Intrinsic factors

Extrinsic factors

Age Occupation
Vascular Sport


Physical Load

Anatomical variants

Training errors

Joint laxity Shoes and equipment
Muscle weakness Environmental condition



 (Ahmad, Z et al 2019)


Tendinopathies have been poorly understood due to the little efficacy or inconsistencies we have seen with prior methods of research experiments and clinical treatments. Despite the methodological improvements in the last few decades regarding tendon health and treatment, we still see a gap in research. Many experiments in developed tendon research have primarily targeted animal species. Though, we do accumulate an abundance of information within the histopathology and healing phase, we don’t take account that the studies are often performed on young (>12 weeks) animals (usually rats). For example, we see increased mRNA expressions of collagen inducing growth factors and collagen type I and III in 2-3 weeks in tendons of rats. However, the carry over to adult humans (>18 YO), remains unknown. As it appears, the human tendon tissue is less responsive to that of a small animal in growth phase. (Heinemeier, K et al 2013) (Magnusson, S et al 2019) This data suggests that animals have a greater potential of growth and cell proliferation in tendons in comparison to humans. Nevertheless, as new studies emerge, it will be possible to develop more effective strategies for interpretation of pathophysiological changes. As we currently understand, both extrinsic and intrinsic factors influence in the health and the propensity to injury. The best treatment for tendon pathology continues to elude scientific data. Understanding tendon tissue adaptions can better suit adequate guidelines for training, treatment, and rehabilitation. Read Part 2 to better understand these concepts and how to apply them.














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