The document explores lower extremity tendinopathies in sports, defining key terms like tendinosis and tendinopathy and discussing the pathology, anatomy, and biomechanics of tendons. It highlights the debate regarding inflammation in tendinopathy, indicating that while traditional views suggest no inflammatory cells are present, recent studies challenge this perspective. It concludes with treatment approaches, emphasizing conservative methods before considering surgery.

1. Lower Extremity tendinopathies
in Sports
Bradd G. Burkhart, MD
Orlando Orthopaedic Center
Sports Medicine

2. Overview
• Terminology
• Anatomy
• Pathology
• Specific Tendinopathies

3. Is it an -itis or an -osis?
• The term tendinitis is considered a misnomer given the lack of
inflammatory cells in tendinopathy histologically
• Many studies use samples from patients that are already symptomatic,
which may mean that the tendon is chronically degenerated (more on
this point later!)
• Tendinosis describes the process of tendon degeneration that is seen
in overuse tendon injuries
• Tendinopathy is a generic term that describes the clinical conditions
in tendons that arise from overuse

4. • So tendinopathy describes the
clinical condition
• When you look at a tendon
that is chronically overused,
the histopathology is
tendinosis
• Recent studies (more later)
that examine acute
tendinopathy do reveal
inflammatory cells
(tendinitis)

5. Anatomy
• Tendons are brilliant white in color
• Cord, strap, ribbon, or band-like
• Tenoblasts (immature tenocytes) and tenocytes constitute 90-95% of the cellular elements of
tendons
• The remaining 5-10% include chondrocytes, synovial cells, etc
• The oxygen consumption of tendons is low, and the ability to work under anaerobic conditions
is great for carrying loads and maintaining tension for long periods but not great for healing!
• Tendons are approximately 70% water
• Type I Collagen (its a question on every ortho test!)

6. Anatomy

7. Tendon-bone junction
• Dense tendon
• Fibrocartilage
• Mineralized fibrocartilage
• Bone

9. Anatomy
• Bloods Supply to tendons
• Intrinsic at the muscle and bone junction
• Extrinsic through paratenon and synovial sheath
• Vascularity is compromised at junctional zones and areas
of stress
• Nerve Supply
• Nerves traverse the paratenon and terminate at the
epitenon

10. Biomechanics
• Tendons are highly
flexible, elastic and
mechanically strong
• They are viscoelastic
and therefore follow
the stress/strain curve
we all know and love!

12. Pathology
• Rupture
• Tendinopathy

13. Rupture
• Acceleration-deceleration mechanism is the most common
(90% of tendon ruptures)
• Etiology is unclear
• Most ruptures of tendons will reveal degenerative
tendinopathy suggesting that the tendon was abnormal prior
to the rupture even if not symptomatic

14. Tendinopathy
• Overuse injuries are generally multifactorial
• Intrinsic and extrinsic factors play a role
• Excessive loading of tendons is the main pathological stimulus for
degeneration
• Tendons respond to overloading with inflammation in the sheath,
degeneration of the tendon proper, or both
• Unless fatigue damage is actively repaired, tendons will weaken and
eventually rupture

15. tendinopathy
• Etiology of tendinopathy is not clearly understood
• Ischemia can occur with stressed tendon, reperfusion can
release oxygen free radicals, which can damage the tendon
• Hypoxia itself may cause tenocyte death
• Degeneration may occur as a result of the heat stored and
released by the tendon during vigorous exercise
• Repetitive strain on a tendon may lead to early tenocyte
apoptosis (programmed cell death)

16. • Cytokines (caused by cyclic strain) can cause
degeneration.
• This includes release of COX-2, MMP-1, -3, and
PGE
• COX inhibitors (NSAIDS) work here
• Ciprofloxacin can induce cytokine release, use
of flouroquinolones inhibit tenocyte
metabolism. Associated with rupture and
tendinopathy

17. Tendinosis
• Tendinosis is the pathology seen in tendinopathy
• Histologic examination reveals: “disordered, haphazard healing with
an absence of inflammatory cells, a poor healing response,
noninflammatory intratendinous collagen degeneration, fiber
disorientation and thinning, hypercellularity, scattered vascular
ingrowth, and increased interfibrillar glycosaminoglycans”
• Memorize this and tell your next patient!
• Tendinosis represents failure of the tendon to repair itself in response
to stress

18. Presentation
• Suprisingly, tendinosis does not always lead to symptoms, in fact,
tendinosis is often incidentally noted on MRI
• If pain exists, it can arise not from several possible alternate sources
• Chemical irritants and neurotransmitters
• Substance P
• Glutamate
• The jury is still out!

19. To Add to the confusion...
• A recent study by Millar, et al in AJSM 2010 noted that in early human
tendinopathy, inflammatory cells are indeed present!
• These included mast cells and macrophages
• The samples were from the subscapularis tendons in shoulders with a
supraspinatus tear, controls were from shoulders with no RC pathology
• This is the first study on humans that shows inflammation in early
tendinopathy!
• Studies on rats show similar findings, ie inflammatory cells in early
tendinopathy

20. • So based on years of study, there are no inflammatory cells
in tendinopathy, ie no tendinitis
• This is challenged by a recent study that suggests that
inflammatory cells do exist in early tendinopathy
• Maybe the timing of the samples is the source of the
confusion? Maybe shoulders are different than knees? Can
this study be reproduced?

21. Tendon Healing
• Inflammatory phase: 0-3 days
• Inflammatory cells first, then tenocytes
• Proliferative phase: 3 days-6weeks
• Synthesis of type III collagen
• Remodeling phase: 6 weeks- one year
• Consolidation followed by maturation
• Consolidation phase 6-10 weeks: Collagen becomes organized, type I more
prevalent
• Maturation phase 10 weeks to up to one year: Continued change to scar-like
tendon tissue

22. Specific tendinopathies
• Quad Tendinopathy
• Patella Tendinopathy: “Jumper’s Knee”
• Achilles Tendinopathy
• etc

23. Tendinopathies
• Each of the specific tendinopathies described are easily
diagnosed clinically, in general MRI is not needed initially
• Usually the pain is directly over the tendon itself and each
tendon is easily palpated
• Distinction can be made towards insertional versus
midsubstance
• Treatment is conservative

24. Quad
• Generally associated with an increase in activity (jumping, running,
climbing, etc)
• Point tender over the quad
• Nonoperative management almost always successful
• Operative management only with failure of extensive conservative
care
• Excision of the diseased tendon and bone stimulation
• If greater than 50% involved, repair may be necessary

25. Jumpers Knee
• Deep fibers at the origin of the tendon from the patella most
common site
• Insidious onset
• PT is 90% successful
• Injections are not recommended
• Surgery if all else fails! Excise, debride, stimulate
• Recovery is up to 6-12 months

26. Achilles
• Conservative treatment initially
• NSAIDs, rest, stretching
• Immobilization if needed
• All else fails? MRI to examine extent of involvement,
possible surgical reconstruction

27. Summary
• Tendon is a strong, elastic structure that does not heal well
• Most studies show that no inflammation occurs in
tendinopathy but this is questioned by one recent study
• Tendinopathy is easily diagnosed by not easily treated
• Surgery is utilized only as a last resort

29. references
• Millar, et al. Inflammation is present in early human tendinopathy.
American Journal of Sports Medicine, 2010; 38 (10): 2085-
2091
• Maffulli, et al. Overuse tendon conditions:Time to change a
confusing terminology. Arthroscopy: The Journal of
Arthroscopic and Related Research. 1998; 14(8): 840-3.
• Sharma, et al. Tendon injury and tendinopathy: Healing and repair.
Journal of Bone and Joint Surgery. 2005; 87-A(1):187-202
• Johnson, D. Editor, Clinical Sports Medicine, 2006.