© ISAKOS 2017
Gian Luigi Canata, Pieter d’Hooghe and Kenneth J. Hunt (eds.)Muscle and Tendon Injuries10.1007/978-3-662-54184-5_1111. Why the Tendon Tears and Doesn’t Like to Heal
(1)
Department of Biomedical Sciences for Health, University of Milan, Milan, Italy
(2)
1st Department, Azienda Socio Sanitaria Territoriale Centro Specialistico Ortopedico Traumatologico Gaetano Pini-CTO, Milan, Italy
Keywords
Tendon healingTendon tearsAbbreviations
AGEs
Advanced glycation end products
HP
Hyperparathyroidism
NSAIDs
Nonsteroidal anti-inflammatory drugs
PTH
Parathyroid hormone
11.1 Introduction
Tendons are part of the musculotendinous unit, and their main function is to transfer the muscular tension to the bone levers.
The homeostasis of tendons is a critical aspect. An unbalanced relation between regenerative and degenerative processes can predispose to tendon tears (Sharma and Maffulli 2005), which are common conditions that every physician treating musculoskeletal system disorders will face throughout his career (Paavola et al. 2005).
Numerous intrinsic and extrinsic factors can interfere with tendon homeostasis, creating a disequilibrium and leading to tendon weakening.
Some of these factors are irreversible; others can be modified by a correct medical approach. In order to properly treat such patients with weakened tendons, a complete knowledge of the matter is therefore crucial.
11.2 Intrinsic or Extrinsic Factors Leading to Tendon Tears
11.2.1 Intrinsic Factors
11.2.1.1 Anatomical Factors
The mechanical forces generated by muscle contraction are transmitted to the bones via tendons. Sheets of connective tissue, surrounding tendon components, define the tendon structure (Benjamin et al. 2008; Franchi et al. 2007; Maffulli et al. 2005).
This complex and hierarchical structure guarantees an appropriate transmission of pulling forces to rigid collagen fibers through elastic elements. As a result, tendons are remarkably strong and can withstand high tensions (Nickisch 2009).
Tendons have relatively low cellularity. There are two different mature cell types located between the collagen bundles: tenocytes and tenoblasts.
The vascularization also plays a key role in the pathophysiology of the tissue and is very variable. The three different areas of the tendon have different blood supply (Maffulli et al. 2005; Arverud et al. 2016). The musculotendinous junction is vascularized by separated arteries that provide blood flow to both tendon and muscle tissues. There are no anastomoses between these branches. Arteries and veins run transversally to the long axis in the paratenon and vascularize the midpart of the tendon via endotenon through arterioles and venules (Arverud et al. 2016).
There is a fibrocartilaginous layer interposing between the different tissues of the tendon-to-bone junction, and there is no straight communication among the different tissues.
Different tendons show different weak points according to their vascularization pattern. The Achilles tendon, for example, presents an area of lowest blood supply from 2 to 6 cm proximally to its bone insertion. Tendon tears usually occur in this area (Arverud et al. 2016; Knobloch 2008).
The area of deficiency in the rotator cuff is generally situated 7–10 mm far from the tendon-to-bone junction, where there is a lack of communication between the vascularization systems (Ling et al. 1990).
Due to vascularization flaws, low cellularity, and the great forces involved, it is anatomo-physiologically evident how the balance between regenerative and degenerative processes can be compromised (Sharma and Maffulli 2005; Maffulli et al. 2005; Arverud et al. 2016; Ling et al. 1990; Aström and Westlin 1994).
11.2.1.2 Aging
Tendon tears usually occur in middle-aged and older patients when the involved forces exceed the tolerated ones (Paavola et al. 2005). A physiological deterioration is expected in aging tendons resulting in weakened structure and function that can lead to tendon stiffness. It is a universal process that involves the different components of the tissue (Tuite et al. 1997; Kubo et al. 2001). During aging fibroblastic activity of tenoblasts is decreased, as the number of total cells (Nakagawa 1996).
In some cases, calcification could further weaken the tendon tissue and contribute to ruptures. In effect, some authors well described the progression of calcifying tendinitis to rotator cuff tears (Gotoh et al. 2003; Hsu et al. 1994; Uhthoff and Sano 1997). The effect of aging on the vascularization of the tendon is a reduction of vessels per unit of surface area (Tuite et al. 1997).
When the patient ages, the physical requests to the musculoskeletal system decrease. This mimics the disuse of tendons (reduced loading), thus a physiological weakening due to a catabolic state (Waugh et al. 2012; Dideriksen et al. 2016).
Such a mixture of depletions makes the tendon more vulnerable to damages.
11.2.1.3 Pathologies
Several pathologies have been associated with tendinopathy and tendon tears. The most accurately described ones are hyperparathyroidism, gout, obesity, diabetes, and vasculopathies (Ackermann and Hart 2016).
Hyperparathyroidism (HP) is a multisystemic disease caused by an excessive release of parathyroid hormone (PTH). The consequences are abnormal blood values of calcium and phosphate. It compromises the renal and neurological functioning, and musculoskeletal manifestations are often described (Pappu et al. 2016). Calcium deposits imply manifestations such as condrocalcinosis, arthralgias, and calcifying tendinitis that can be the cause of tendon tears (Pappu et al. 2016; Gao et al. 2013).
The correlation between high level of uric acids and consequently monosodium urate crystal deposition of gout and tendinopathies has been recently investigated by Andia and Abate (2016). The inflammatory response ruled by the IL-1β can interfere with tendon homeostasis, but further investigations, regarding the effects of crystals on tendon cells and innate immunity, still need to be done (Andia and Abate 2016; Taniguchi et al. 2014).
When the optimal vascularization and innervation of tendons decline, pathological features can occur. Diabetes and vasculopathies, being related to peripheral vasculo-nervous impairment, have been epidemiologically associated with tendinopathy (Abate et al. 2013a, b; Ackermann 2013).
Obesity has multiple and demonstrated harmful effects on tendons (Wearing et al. 2013; Wise et al. 2012). A significant increase in weight-bearing exponentially intensifies tendon stress. Furthermore, obese patients present systemic factors with a significant relevance in the pathogenesis of tendon tears (Ackermann and Hart 2016). Adipocytes produce factors such as chemerin and leptin that affect mesenchymal cells function, thus tissue turnover.
Additional damage to the tendon structure of collagen fibers is guaranteed by high AGEs (advanced glycation end products) derived from glucose catabolism (David et al. 2014; Franceschi et al. 2014; Abduljabbar et al. 2016). Abate et al. recently described how these metabolites develop stable covalent cross-links within tendon fibers (2013a).
11.2.2 Extrinsic Factors
11.2.2.1 Trauma and Overload Injuries
According to different loading and different anatomical regions, tendons are variously involved in overloads or trauma. Stressful situations can disclose subclinical compromised tendons due to aging, anatomical abnormalities, or comorbidities (Maffulli et al. 2005).
Direct trauma described as injuries resulting from direct impact can cause tendon ruptures. Nevertheless, more often an indirect trauma, such as an eccentric loading on muscle levers, leads to the tear.
The most often ruptured ones are the Achilles tendons, the quadriceps tendons, the rotator cuff tendons, and the biceps tendons (Paavola et al. 2005).
The pathophysiology of overuse injuries associates recurrent overloading to tendinosis/tendinitis which can proceed to micro-injuries and ultimately to a complete rupture (Kannus and Józsa 1991). Typically observed in sport and working environments, overuse injuries are a more complex field involving numerous aspects, organized by Paavola et al. in intrinsic and extrinsic factors (2005).
Intrinsic factors are muscular imbalance, muscular weakness, malalignments, limb length discrepancy, and lack of elasticity.
Extrinsic factors are training errors (distance, intensity, hill work, technique, fatigue), playing fields (consistency and irregularity), difficult environmental conditions, footwear, and equipment.
Since physical activity is practiced by people of all ages nowadays, the prevention of excessively stressful events is mandatory. In middle-aged and older patients, these events can lead to definitive rupture.
11.2.2.2 Drugs, Alcohol, and Smoking
Mainly four classes of drugs can cause tendon degeneration: in particular glucocorticoids and quinolones are better studied, while aromatase inhibitors and statins still need deeper evaluations (Kirchgesner et al. 2014).
Corticosteroids, often used as anti-inflammatory drugs in musculoskeletal disorders, have catabolic features on tendon homeostasis resulting in inhibition of new collagen and proteoglycan formation (Scutt et al. 2006). Preclinical and clinical studies have shown how glucocorticoid injections affect the biology of tendons reducing cellular turnover and, eventually, the energy to failure of the tissue (Scutt et al. 2006; Dean et al. 2014a, b; Hossain et al. 2008).
Quinolones are broad-spectrum antibiotic drugs and have toxic effects on tendons. The pathological relation between fluoroquinolones and tendon ruptures has been studied and proved by van der Linden et al. in the IMS Health database (2002). Their findings show that rupture events are rare but existing and also indicate that corticosteroid association can enhance tendon tears. These unfortunate accidents usually occur in Achilles tendon (van der Linden et al. 2002; Hori et al. 2012).
Passaretti et al. recently underlined and described the existing association between tendon failures and alcohol consumption (2016). Particularly, massive rotator cuff tears were related to high alcohol intake which is a risk factor for tendon injuries in both sexes (Passaretti et al. 2016).
11.3 Factors Affecting Tendon Healing
There are distinct stages of tendon pathology, from mild tendinopathy to complete tendon ruptures. In all these clinical conditions, tendon healing is a multifactorial process involving different actors who play various roles. Blood-derived cells, tissue-derived cells, and neurovascular and inflammatory mediators concur to regulate the three phases of tissue regeneration: inflammatory, reparative, and remodeling.
The medical approach to the injury can be either surgical or conservative according to the entity and the location of the trauma. The integrity of blood vessels is as essential as the close contact of tendon stumps. Surgeons should not be traumatic on bloody supplying structures while performing surgeries. Once these conditions are satisfied, the physiological processes can start.
The postoperative role of the physician is to guide patients through optimal rehabilitation without inhibiting tendon healing.
In addition to the intrinsic and extrinsic factors, there are further considerations that need to be evaluated while dealing with tendon healing.
11.3.1 Biomechanical Factors
The balance of loading stimuli during the healing of torn tendons is a matter of discussion in the field of musculoskeletal disease. The mechanobiology of tendon regeneration processes is well described by Killian et al. (2012). They described how postoperative rehabilitation can space from a total immobilization to passive motion to, eventually, overuse and from an environment leading to a catabolic state to another one leading to further micro-damages, respectively.
Several studies have shown how biological disuse of tendon can enhance the deterioration processes (Dideriksen et al. 2016; Killian et al. 2012; Bring et al. 2007). Preclinical animal models compare a healthy limb to the immobilized contralateral (Bring et al. 2009). Immobilization has been achieved by denervation, botulinum injection, or long-term immobilization with cast. These studies evince the biological reasons of tendon weakening after disuse. Metabolic activity and primary gene response decrease. In addition, the expression of sensory neuropeptide receptors guiding neuronal plasticity declines.
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