12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

Anatomy, Tendons
Bruno Bordoni; Asa C. Black; Matthew Varacallo.

Author Information and Affiliations

Last Update: May 1, 2024.

Introduction
The tendon is a "mechanical bridge," transmitting muscle forces to the bones and joints. This tough, fibrous structure also helps
muscles complete joint movements along a plane. The tendon type reflects its associated muscle's morphology and function.
Tendon tissue is present throughout an entire muscle's length, not only the tips. The muscle's connective tissue layers
(epimysium, perimysium, and endomysium) merge to attach to one or more fixed osseous points. Tendon tissue close to the
muscle has contractile fibers. The muscle influences tendon activity, and in turn, the tendon impacts how the muscle functions.

Healthcare professionals must consider these important relationships, especially when performing manual therapy, rehabilitation,
and surgery. Tendon tissue architecture can adapt to physiological (eg, training) or pathological (eg, traumatic) stimuli influenced
by systemic, hormonal, environmental, and age-related factors.[1][2]

Structure and Function

Tendons play an extraordinary role in mechanics and movement. These structures transmit muscle forces to the skeletal levers to
facilitate movement and body posture maintenance. Tendons enable muscles to maintain optimal distance from the joint they
operate on without needing excessive muscle length between their origin and insertion points. Tendons are stiffer than muscles,
have greater tensile strength, and can withstand large loads with minimal deformations. These properties enable tendons to
transmit muscle forces to bones efficiently, minimizing energy loss from tendon stretch (see Images. Extrinsic Foot Muscles and
Foot Sole Tendons and Ligaments). For example, the foot's flexor tendons can bear more than 8 times the body weight and store
about 40% of this weight for elastic hysteresis during walking.[3][4][5][6]

Tendon Sheaths

Tendon sheaths are auxiliary structures that primarily aid in the smooth movement of tendon tissue between neighboring
structures and prevent deviation during muscle contraction.
https://www.ncbi.nlm.nih.gov/books/NBK513237/ 1/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

Fibrous Sheaths

Showers and bone incisions typically have a fibrocartilaginous floor covered by a fibrous fabric roof forming a bridge. This
structure, known as the fibrous sheath or retinaculum, is commonly found in the extremities. Examples include the retinacula of
the flexor and extensor tendons in the hand and foot at the wrist and instep levels (see Image. Forearm Extensor Muscles and
Tendons). Fibrous sheaths, or retinacula, serve as channels for tendon movement, especially for long tendons. These structures
prevent significant friction on neighboring tissues, particularly at bone structures, ensuring smooth sliding action. These regions
contain tunnels with synovial sheaths surrounding the tendons.[7]

Synovial Sheaths

The synovial sheaths facilitate tendon sliding within the fibrous sheath (see Image. Flexor Tendon Anatomy). These structures
comprise 2 thin serous sheets: the parietal sheet covering the fibrous sheath's walls and the visceral sheet covering the tendon's
surface. These sheets extend to both ends, enclosing a space with peritendinous fluid that serves mainly as a lubricant.
Additionally, loose tissue peduncles detach from osteofibrous canal walls, terminating on the tendon belly and housing vessels
and nerves. These structures, collectively called the "mesotenonium," are also covered by synovium and vary in number
depending on tendon length. True synovial sheaths are only found in areas necessitating highly efficient lubrication due to
sudden direction changes and increased friction.

Peritendon Sheaths (Paratenon)

The peritendinous sheets have overlapping functions with the synovial sheaths despite their histological differences. The
paratenonium (paratenon) is composed of type I and type III collagen fibrils and thin elastic fibers. This structure reduces
friction and works like an elastic sleeve, allowing free tendon movement within its environment.[8]

Reflection Pulleys

Reflection pulleys are thickened regions of dense fibrillar tissue found within fibrous sheaths, encasing tendons within the
sliding bed, particularly around tendon curves. These structures facilitate smooth tendon movement.[9]

Tendon Bursae

Tendon bursae help minimize friction between the tendon and adjacent bony structures (see Image. Medial View of the Knee).
Bursae are small serous vesicles situated where bony protrusions might compress and cause friction on tendons, potentially
leading to wear and tear. Examples are the subacromial, infrapatellar, and retrocalcaneal bursae.[10]

https://www.ncbi.nlm.nih.gov/books/NBK513237/ 2/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

Deep to the paratenon, the entire tendon is surrounded by a thin, dense connective tissue sheath called "epitenonium" (epitenon).
The paratenon and epitenon are collectively called "peritenonium." Collagen fibrils within the epitenon are oriented transversely,
longitudinally, and obliquely. The epitenon fibrils occasionally appear fused with the superficial tendon fibrils.

The epitenon is connected to the peritenonium externally and endotenonium (endotenon) internally. The endotenon, a thin
membrane consisting of loose connective tissue, covers and organizes individual tendon fibers into larger units bundled in
various orders. This membrane separates different collagen bundles, allowing neurovascular penetration within the tendon
(see Image. Tendon Hierarchical Structure Schematic Diagram).

The musculotendinous junction is the point where the muscle pierces the tendon. The osteotendinous junction is the point where
the tendon inserts on the bone.[11][12]

Cell Population and the Extracellular Matrix

Tenocytes and tenoblasts are specialized fibroblasts that coexist in tendinous tissue. Tenocytes are elongated, while tenoblasts
are ovoid. Tenoblasts represent approximately 90% to 95% of tendon fibroblasts. These specialized fibroblasts produce
extracellular matrix components, including collagen and proteoglycans.[13] Collagen makes up approximately 65% to 80% of
the extracellular matrix. The predominant collagen type in tendons is type I. Type III collagen is present in the epitenon and
endotenon. Type II collagen occurs in the osteotendinous junction's fibrocartilaginous areas. Elastin, proteoglycans, and
glycoproteins constitute 4%, 4%, and 2% of the extracellular matrix, respectively.

Tendons consist of collagen fibers arranged parallel to each other and the tendon axis. The bundles of collagen fibers show a
wavy pattern with periodic orientation changes known in the literature as crimps. Crimps vary in size and shape within the same
tendon, often resembling isosceles or scalene triangles of different dimensions. When observed through a scanning electron
microscope, a single crimp is composed of straight fibrillary segments closely packed and connected by nodes or hinges. All
fibrils within each fascicle simultaneously change direction at these points. Rather than forming a loop, the fibrils deform
similarly to a hollow cylindrical structure. Collagen bends but does not break.[14]

Healing occurs in multiple overlapping phases after a tendon injury. Tenoblasts deposit collagen fibers during the healing phase
and transform into tenocytes in the last repair phase.

Mechanical Properties

A tendon's biomechanical behavior is related to its shape and the magnitude of the tension applied to it. Muscles like the finger
flexors that perform delicate and precise movements possess long and thin tendons. In contrast, muscles for actions of power and
endurance, such as the quadriceps femoris and triceps surae, have shorter and more robust tendons. A short tendon's tensile

https://www.ncbi.nlm.nih.gov/books/NBK513237/ 3/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

strength is greater than a long tendon, tolerating more loads with the same diameter. Meanwhile, a long tendon can withstand
greater deformation than a short tendon. A tendon's strength and resistance rely on its diameter and length. Tendons'
biomechanical properties are linked to collagen fibril diameter and arrangement. Tendons subjected to high stress have fibrils
with a larger diameter, which are less flexible than smaller ones.

Tendons' capacity to absorb and transmit muscle forces is linked to their crimps. Research reveals that higher tendon loads
produce wider angles at a crimp's base. Tendon stretch gradually flattens the crimps, which act as shock absorbers during the
initial pulling stages. Afterward, the crimps allow the tendon to regain its shape when force application ceases. Crimp flattening
occurs gradually from the outer edges to the center.

Adaptation to Mechanical Stress

Tendinous adaptations differ between genetic sexes. Genetic females develop less tendon strength but greater length than genetic
males when subjected to repeated mechanical stress. The reasons for this tendency are poorly understood.

Tendinous tissue adapts to its mechanical environment. Adaptation is stress-specific. Mechanical tension from muscle
contraction and relaxation increases collagen synthesis and tendon diameter. Tendon stiffness and the Young modulus increase
with continued tension. The Young modulus is the ratio of tensile stress to tensile strain, expressed in pressure units. This ratio
defines how easily the tendon can stretch and deform.[15]

Effect of Aging

The tendons' ability to adapt decreases with age. Aging alters cellular structure and diminishes tendons' capacity for
regeneration. Moreover, tendons become less effective in directing muscle forces toward the bone tissue. Collagen fibers become
less organized, and calcification can occur. Fibroblasts decrease, and senescent cells appear. Water content and proteoglycans
decrease. All these changes reduce tendons' viscoelasticity and strength and increase trauma susceptibility. Decreased estrogen
levels in older women loosen tendinous tissue, making it more prone to traumatic injury and inflammation.[16][17]

Embryology
The tendon arises from the ectoderm and mesoderm. Tendons primarily originate from neural crest cells of the ectoderm and the
paraxial and lateral plate mesoderm, giving rise to the craniofacial, axial, and limb tendons respectively.[18] Animal
models show that cranial and limb tendons form independently from muscle tissue. By comparison, muscle progenitors are
required to move the axial tendon precursors from their origin to their destination under the influence of fibroblast growth factor.
[19] The progression of cartilage and muscle tissue in the developmental period typically occurs more quickly than the tendon.

https://www.ncbi.nlm.nih.gov/books/NBK513237/ 4/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

Blood Supply and Lymphatics

Tendons have a complex vascular supply. Blood vessels supplying the tendon may originate from the muscle belly, the
periosteum around the osteotendinous junction, or the vascular networks within peritendinous leaflets or synovial sheaths.[20]
[21]

Peritendinous leaflets' circulatory networks vary within and between tendons. These networks may feature primary trunks
forming either a mesh structure or irregularly arranged concentric arches, with small to medium-sized arteries and 1 or 2 satellite
venous connections.

Three types of microvascular capillary units exist within tendons. One involves capillaries traveling a long distance parallel to
the tendon's longitudinal axis before looping back to join a venule. Another type originates from a single arteriole, giving rise to
several capillary loops running in different planes within the tendon. The 3rd type functions as arteriovenous shunts, featuring
short capillaries with a straight course. Variability in these microvascular units' organization facilitates gas and metabolite
diffusion within individual tendon bundles.

Tendinous lymphatic drainage exists as a network, with lymph draining toward tendon veins or other neighboring venous
structures. Blood flow to the tendon rises under mechanical stress, but lymphatic drainage does not increase proportionally.

Nerves
Tendons are innervated by nerve branches from the muscle belly and skin, though innervation is scarce. Nerves are localized to
the paratenon, endotenon, and epitenon. Nerve branches parallel the tendon's central axis, connecting with transverse and
oblique branches. Golgi tendon organs, Pacini or Ruffini corpuscles, and free arborizations lie in the nerve endings.[22]
Innervation accompanies the vascular supply. Tendons' sympathetic innervation mirrors the vascular supply, serving to induce
vasoconstriction. Sensory fibers similar to parasympathetic nerves or separate small-diameter sensory fibers stimulate
vasodilation.

Muscles
The tendon adapts to its associated muscle's morphology. Flat muscles have flattened tendons or aponeuroses, while round ones
have cordiform tendons. Healthy tendons enable muscles to function effectively and adapt to competing demands. Such tendons
also facilitate optimal mechanotransduction mechanisms in contractile fibers, enhancing overall performance.

Physiologic Variants

https://www.ncbi.nlm.nih.gov/books/NBK513237/ 5/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

Tendon anatomy variations are common. For instance, the tendon of the biceps brachii's long head can vary in shape and origin
or even be absent, with a prevalence ranging from 1.9% to 7.4% in the population.[23] The popliteal muscle tendon bifurcates,
producing 2 muscular bellies, in approximately 0.4% of individuals.[24] Length and shape variability of the flexor hallucis
longus tendon is seen in about 9.8% of cases.[25] The patellar tendon, which stabilizes the patella, may appear as 2 distinct
tendons or be absent.

Surgical Considerations
Tendon injuries may be managed conservatively or operatively. The decision to perform surgery depends on many factors.
A review of specific tendon injury management is beyond the scope of this activity. However, the key principles guiding the
comprehensive clinical analysis and management of diverse tendon injuries include the following:

Injury severity, ie, partial or complete

Body region affected

Capacity of the surrounding structures to compensate (to assess the clinical impact of a tendon injury and predict
functional outcome)

Patient age

Functional goals (sedentary versus active or sport-involved lifestyle)

Patient medical comorbidities (diabetes, inflammatory arthropathies, systemic conditions)

Hand dominance

Resulting cosmetic deformity

Injury chronicity and resulting tissue quality (warranting consideration of direct repair versus allograft or autograft tendon
reconstruction)

Available surgical alternatives (navigating tendon transfer principles)

Social factors (patient compliance, smoking status, history of illicit drug use)

Current medications (chronic steroid use, fluoroquinolones)

Clinical Significance
https://www.ncbi.nlm.nih.gov/books/NBK513237/ 6/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

Tendinopathy

Tendinopathy results in vascular changes and adaptations to the muscle and tendon's macroscopic and microscopic environment.
Increased vascularization is due to hypertrophy and hyperplasia induced by an angiogenic cytokine, such as vascular endothelial
growth factor (VEGF). Inflammation due to injury increases local VEGF concentrations. Greater perfusion reduces tendon
strength by decreasing the sliding capacity of its various connective layers. Nerve fibers also increase superficially in the tendon
and deeper structures. Nociceptive nerve branches also proliferate, causing pain.[26][27][28][29] Sympathetic nerve fibers also
multiply near the blood vessels. Research suggests that altered tenocytes may produce nociceptive neurotransmitters, which can
subsequently trigger pain signals recorded by the sympathetic nervous system.

Ehlers-Danlos Syndrome

Ehlers-Danlos Syndrome (EDS) is a group of genetically borne connective tissue disorders that result in abnormal collagen
synthesis, increasing skin elasticity and joint mobility. Collagen gives strength and elasticity to connective tissues, including the
components of tendons, joints, skin tissue, and blood vessels. EDS incidence is approximately 1 in 5000 cases.[30][31] The
condition develops in childhood but is often undiagnosed until later in life.

EDS' clinical manifestations vary widely. Thus, disease severity also differs individually. Diagnosis hinges on medical history
and physical examination, noting the patient’s movements.[32] Symptoms may include abnormal scar formation, stretchy skin,
and loose joints.

Joint hypermobility or laxity is characteristic of EDS. Small joints are typically more affected than large joints. Joint pain,
dislocations, and sprains are common. Other EDS complications include scoliosis, osteoarthritis, chronic pain, and aortic
dissection.

Thirteen EDS subtypes have already been identified, with 19 known causal genes involved in extracellular matrix and collagen
development. Inheritance is often autosomal dominant. Collagen abnormalities are present in most known EDS variants.

Classical EDS, consisting of former types I and II, is characterized by abnormal type V collagen production. Vascular EDS,
formerly EDS type IV, exhibits abnormal type III collagen. This EDS type is the deadliest, as it can manifest with arterial
rupture, though only 4% to 5% of patients have this variant. Arthrochalasia EDS, comprised of former types VIIA and VIIB,
exhibits type I collagen deficiencies. Cardiac-valvular EDS also involves collagen type I abnormalities, though this condition is
autosomal recessive and may present with severe cardiac valve defects. Myopathic EDS is associated with collagen type XII
abnormalities and manifests with congenital muscle atrophy, proximal joint contractures, joint hypermobility, and developmental
motor delay. The causative gene of hypermobile EDS, formerly type III EDS, is unknown in most cases, though a few
individuals have tenascin-X and type III collagen mutations. This EDS variant is the least severe and most common.[33]
https://www.ncbi.nlm.nih.gov/books/NBK513237/ 7/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

Diagnosis of EDS is difficult because joint hypermobility is multifactorial, with gender, age, training, and body weight all
contributing to the symptom. Patients with hypermobile EDS exhibit joint hypermobility, dislocation, and cutaneous
manifestations. Additional symptoms include chronic pain, fatigue, anxiety, and dysautonomia. The musculoskeletal pain
associated with this condition is often diagnosed as fibromyalgia.

Pain is a common EDS symptom, which may present as variable arthralgias during childhood. Concurrent pain patterns, such as
paresthesias, burning sensations, allodynia, cramps, and myalgias, may suggest a neurological component alongside joint and
skin pathologies. Small fiber neuropathy is common.[34] Pain may be classified as nociceptive, arising from pain receptor
stimulation, or neuropathic, caused by nerve dysfunction. Musculoskeletal nociceptive pain occurs in EDS, but neuropathic pain
seems more common.[35] Pain may also be initially nociceptive, but neuropathic pain can become a significant factor as pain
intensifies. Central sensitization is also significant, indicating a generalized hyperalgesia among patients. Loss of proprioception,
muscle weakness, and alterations in the extracellular matrix further contribute to chronic pain and its perpetuation.[36]

Patients with EDS often present with chronic, severe pain. The condition must be differentiated from other genetic connective
tissue syndromes such as Marfan syndrome, cutis laxa, and skeletal dysplasias.

Marfan Syndrome

Marfan syndrome is an autosomal dominant connective tissue disease with variable penetrance, resulting in many symptoms.
The most dangerous complications of this condition include aortic dissection and regurgitation (see Image. Marfan Syndrome-
Associated Aortic Regurgitation). The primary genetic abnormality is a mutation in the fibrillin-1 gene, the product of which
coats elastins.[37] Musculoskeletal system abnormalities are often the presenting physical signs of Marfan syndrome. Increased
joint laxity, excessive long bone growth, scoliosis, and sternal deformities such as pectus excavatum are common.

The Steinberg or “thumb sign” may indicate Marfan syndrome during the physical examination. The sign is positive if the entire
distal phalanx of the thumb protrudes beyond the hand's ulnar border while the thumb is abducted with the fingers curled over it.
The Walker-Murdoch or “wrist" sign is evaluated by having the patient encircle the wrist proximal to the styloid process with the
thumb and finger of the other hand. This sign is positive if the thumb overlaps and completely covers the nail of the encircling
digit.[38]

Other Issues
Tendon tissue plays a crucial role in fascial continuity, actively and passively contributing to muscle performance and joint
movements.[39][40] The tendon-bone junction typically lacks nerves, yet a loss of innervation in the rest of the tendon can lead
to chronic tendinopathies, especially near such junctions.[41]

https://www.ncbi.nlm.nih.gov/books/NBK513237/ 8/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

Review Questions

Access free multiple choice questions on this topic.

Comment on this article.

Figure

Extrinsic Foot Muscles. This medial view of the right foot shows the tendons of
the tibialis anterior, tibialis posterior, flexor digitorum longus, extensor hallucis longus,
and flexor hallucis longus. The retrocalcaneal bursa, tendo calcaneus (more...)

Figure

Foot Sole Tendons and Ligaments. This illustration shows the anatomic relationships
between the plantar intermetatarsal, calcaneocuboid, tarsometatarsal, cuneonavicular,
cuboideonavicular, and calcaneonavicular ligaments. The long plantar ligament
(more...)

Figure

Forearm Extensor Muscles and Tendons. This illustration shows the anatomic
relationships between the extensor pollicis longus, extensor indicis, extensor carpi
ulnaris, extensor digitorum communis, extensor carpi radialis, extensor carppi radialis
longus, (more...)

https://www.ncbi.nlm.nih.gov/books/NBK513237/ 9/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

Figure

Medial View of the Knee. The image shows the relationship between the tendons that
form the pes anserinus and the anserine bursa, implying a difficult clinical and imaging
diagnosis. Helfenstein Jr M, Kuromoto J. Anserine syndrome [in Portuguese]. Rev
(more...)

Figure

Flexor Tendon Anatomy. This image shows the synovial lining around the tendons
within the pulley systems at the wrist and digits. Referenced from Figure 30-1 of
Musculoskeletal Key https://musculoskeletalkey.com/flexor-tendon-injury/

Figure

Tendon Hierarchical Structure Schematic Diagram. This illustration shows how the
tendon's collagen triple-helix strands are organized into microfibrils, fibrils, fibers, and
fascicles, then covered by the endotenon, epitenon, and paratenon. Meeremans (more...)

Figure

Marfan Syndrome-Associated Aortic Regurgitation. Shown in this image is aortic root

dilatation in a patient with Marfan syndrome. Contributed by Dr Anam Khan- AIIMS
New Delhi

References
1. Kamrani P, Marston G, Arbor TC, Jan A. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Mar 5, 2023.
Anatomy, Connective Tissue. [PubMed: 30860769]
2. Dave HD, Shook M, Varacallo M. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 28, 2023. Anatomy,
Skeletal Muscle. [PubMed: 30725921]
https://www.ncbi.nlm.nih.gov/books/NBK513237/ 10/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

3. Tiwana MS, Sinkler MA, Bordoni B. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 28, 2023.
Anatomy, Shoulder and Upper Limb, Triceps Muscle. [PubMed: 30725681]
4. Dodson SC, Koontz NA. Spinal Manifestations of Systemic Disease. Radiol Clin North Am. 2019 Mar;57(2):281-306.
[PubMed: 30709471]
5. Kani KK, Chew FS. Terrible triad injuries of the elbow. Emerg Radiol. 2019 Jun;26(3):341-347. [PubMed: 30690677]
6. Tsutsumi M, Nimura A, Akita K. The Gluteus Medius Tendon and Its Insertion Sites: An Anatomical Study with Possible
Implications for Gluteus Medius Tears. J Bone Joint Surg Am. 2019 Jan 16;101(2):177-184. [PubMed: 30653048]
7. Ray G, Sandean DP, Tall MA. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 1, 2023. Tenosynovitis.
[PubMed: 31335044]
8. Schmitt R, Hesse N, Grunz JP. Tendons and Tendon Sheaths of the Hand - An Update on MRI. Rofo. 2022
Dec;194(12):1307-1321. [PubMed: 35705165]
9. Martetschläger F, Zampeli F, Tauber M, Habermeyer P. Lesions of the biceps pulley: a prospective study and classification
update. JSES Int. 2020 Jun;4(2):318-323. [PMC free article: PMC7256895] [PubMed: 32490420]
10. Mercadante JR, Marappa-Ganeshan R. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Oct 8, 2022.
Anatomy, Skin Bursa. [PubMed: 32119325]
11. Steinmann S, Pfeifer CG, Brochhausen C, Docheva D. Spectrum of Tendon Pathologies: Triggers, Trails and End-State. Int
J Mol Sci. 2020 Jan 28;21(3) [PMC free article: PMC7037288] [PubMed: 32013018]
12. Citeroni MR, Ciardulli MC, Russo V, Della Porta G, Mauro A, El Khatib M, Di Mattia M, Galesso D, Barbera C, Forsyth
NR, Maffulli N, Barboni B. In Vitro Innovation of Tendon Tissue Engineering Strategies. Int J Mol Sci. 2020 Sep 14;21(18)
[PMC free article: PMC7555358] [PubMed: 32937830]
13. Makuku R, Werthel JD, Zanjani LO, Nabian MH, Tantuoyir MM. New frontiers of tendon augmentation technology in
tissue engineering and regenerative medicine: a concise literature review. J Int Med Res. 2022
Aug;50(8):3000605221117212. [PMC free article: PMC9393707] [PubMed: 35983666]
14. Franchi M, Fini M, Quaranta M, De Pasquale V, Raspanti M, Giavaresi G, Ottani V, Ruggeri A. Crimp morphology in
relaxed and stretched rat Achilles tendon. J Anat. 2007 Jan;210(1):1-7. [PMC free article: PMC2100258] [PubMed:
17229278]
15. Bianchi E, Ruggeri M, Rossi S, Vigani B, Miele D, Bonferoni MC, Sandri G, Ferrari F. Innovative Strategies in Tendon
Tissue Engineering. Pharmaceutics. 2021 Jan 11;13(1) [PMC free article: PMC7827834] [PubMed: 33440840]
16. Kwan KYC, Ng KWK, Rao Y, Zhu C, Qi S, Tuan RS, Ker DFE, Wang DM. Effect of Aging on Tendon Biology,
Biomechanics and Implications for Treatment Approaches. Int J Mol Sci. 2023 Oct 14;24(20) [PMC free article:
PMC10607611] [PubMed: 37894875]
17.

https://www.ncbi.nlm.nih.gov/books/NBK513237/ 11/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

Chidi-Ogbolu N, Baar K. Effect of Estrogen on Musculoskeletal Performance and Injury Risk. Front Physiol. 2018;9:1834.
[PMC free article: PMC6341375] [PubMed: 30697162]
18. Nakajima T, Ikeya M. Development of pluripotent stem cell-based human tenocytes. Dev Growth Differ. 2021
Jan;63(1):38-46. [PubMed: 33270251]
19. Bobzin L, Roberts RR, Chen HJ, Crump JG, Merrill AE. Development and maintenance of tendons and ligaments.
Development. 2021 Apr 15;148(8) [PMC free article: PMC8077520] [PubMed: 33913478]
20. Kikuchi Y, Sato K, Doita M. An anatomical study of flexor pollicis longus blood supply with specific reference to volar
locking plate surgery. J Orthop. 2020 Jul-Aug;20:119-121. [PMC free article: PMC7000556] [PubMed: 32042238]
21. Jaworski Ł, Zabrzyńska M, Klimaszewska-Wiśniewska A, Zielińska W, Grzanka D, Gagat M. Advances in Microscopic
Studies of Tendinopathy: Literature Review and Current Trends, with Special Reference to Neovascularization Process. J
Clin Med. 2022 Mar 13;11(6) [PMC free article: PMC8949578] [PubMed: 35329898]
22. Frigon A, Akay T, Prilutsky BI. Control of Mammalian Locomotion by Somatosensory Feedback. Compr Physiol. 2021
Dec 29;12(1):2877-2947. [PMC free article: PMC9159344] [PubMed: 34964114]
23. Tarallo N, Morgano MC, Curti M, Spanò E, Castagna A, Genovese EA. Intra-articular long head of the biceps tendon:
magnetic resonance-arthrography classification and review of literature. Pol J Radiol. 2021;86:e93-e101. [PMC free article:
PMC7976233] [PubMed: 33758634]
24. Yoo HJ, Ryu KN, Park JS, Jin W, Park SY, Kang HJ, Kim HS, Kwon GH. Preoperative Meniscus: Pitfalls and Traps to
Avoid. Taehan Yongsang Uihakhoe Chi. 2022 May;83(3):582-596. [PMC free article: PMC9514523] [PubMed: 36238512]
25. Vega J, Redó D, Savín G, Malagelada F, Dalmau-Pastor M. Anatomical variations of flexor hallucis longus tendon increase
safety in hindfoot endoscopy. Knee Surg Sports Traumatol Arthrosc. 2017 Jun;25(6):1929-1935. [PubMed: 28220191]
26. Vlaic J, Josipovic M, Bohacek I, Jelic M. The plantaris muscle: too important to be forgotten. A review of evolution,
anatomy, clinical implications and biomechanical properties. J Sports Med Phys Fitness. 2019 May;59(5):839-845.
[PubMed: 30936418]
27. Cohen PR. Cephalexin-associated Achilles Tendonitis: Case Report and Review of Drug-induced Tendinopathy. Cureus.
2018 Dec 27;10(12):e3783. [PMC free article: PMC6433089] [PubMed: 30915263]
28. Medina Pabón MA, Naqvi U. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 17, 2023. Achilles
Tendinopathy. [PubMed: 30844176]
29. Hassan S, Patel V. Biceps tenodesis versus biceps tenotomy for biceps tendinitis without rotator cuff tears. J Clin Orthop
Trauma. 2019 Mar-Apr;10(2):248-256. [PMC free article: PMC6383069] [PubMed: 30828187]
30. Tinkle B, Castori M, Berglund B, Cohen H, Grahame R, Kazkaz H, Levy H. Hypermobile Ehlers-Danlos syndrome (a.k.a.
Ehlers-Danlos syndrome Type III and Ehlers-Danlos syndrome hypermobility type): Clinical description and natural
history. Am J Med Genet C Semin Med Genet. 2017 Mar;175(1):48-69. [PubMed: 28145611]

https://www.ncbi.nlm.nih.gov/books/NBK513237/ 12/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf

31. Ritelli M, Colombi M. Molecular Genetics and Pathogenesis of Ehlers-Danlos Syndrome and Related Connective Tissue
Disorders. Genes (Basel). 2020 May 13;11(5) [PMC free article: PMC7288446] [PubMed: 32414079]
32. Riley B. The Many Facets of Hypermobile Ehlers-Danlos Syndrome. J Am Osteopath Assoc. 2020 Jan 01;120(1):30-32.
[PubMed: 31904772]
33. Islam M, Chang C, Gershwin ME. Ehlers-Danlos Syndrome: Immunologic contrasts and connective tissue comparisons. J
Transl Autoimmun. 2021;4:100077. [PMC free article: PMC7786113] [PubMed: 33437956]
34. Cazzato D, Castori M, Lombardi R, Caravello F, Bella ED, Petrucci A, Grammatico P, Dordoni C, Colombi M, Lauria G.
Small fiber neuropathy is a common feature of Ehlers-Danlos syndromes. Neurology. 2016 Jul 12;87(2):155-9. [PMC free
article: PMC4940063] [PubMed: 27306637]
35. Camerota F, Celletti C, Castori M, Grammatico P, Padua L. Neuropathic pain is a common feature in Ehlers-Danlos
syndrome. J Pain Symptom Manage. 2011 Jan;41(1):e2-4. [PubMed: 21145199]
36. Guerrieri V, Polizzi A, Caliogna L, Brancato AM, Bassotti A, Torriani C, Jannelli E, Mosconi M, Grassi FA, Pasta G. Pain
in Ehlers-Danlos Syndrome: A Non-Diagnostic Disabling Symptom? Healthcare (Basel). 2023 Mar 24;11(7) [PMC free
article: PMC10094213] [PubMed: 37046863]
37. Zeigler SM, Sloan B, Jones JA. Pathophysiology and Pathogenesis of Marfan Syndrome. Adv Exp Med Biol.
2021;1348:185-206. [PMC free article: PMC8915437] [PubMed: 34807420]
38. Pollock L, Ridout A, Teh J, Nnadi C, Stavroulias D, Pitcher A, Blair E, Wordsworth P, Vincent TL. The Musculoskeletal
Manifestations of Marfan Syndrome: Diagnosis, Impact, and Management. Curr Rheumatol Rep. 2021 Nov 26;23(11):81.
[PMC free article: PMC8626407] [PubMed: 34825999]
39. Bordoni B, Myers T. A Review of the Theoretical Fascial Models: Biotensegrity, Fascintegrity, and Myofascial Chains.
Cureus. 2020 Feb 24;12(2):e7092. [PMC free article: PMC7096016] [PubMed: 32226693]
40. Bordoni B, Mahabadi N, Varacallo M. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 17, 2023.
Anatomy, Fascia. [PubMed: 29630284]
41. Rajpar I, Tomlinson RE. Function of peripheral nerves in the development and healing of tendon and bone. Semin Cell Dev
Biol. 2022 Mar;123:48-56. [PMC free article: PMC8589913] [PubMed: 33994302]
Disclosure: Bruno Bordoni declares no relevant financial relationships with ineligible companies.

Disclosure: Asa Black declares no relevant financial relationships with ineligible companies.

Disclosure: Matthew Varacallo declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

https://www.ncbi.nlm.nih.gov/books/NBK513237/ 13/14
12/9/24, 2:58 PM Anatomy, Tendons - StatPearls - NCBI Bookshelf
This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) (
http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are
not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK513237 PMID: 30020609

https://www.ncbi.nlm.nih.gov/books/NBK513237/ 14/14