Bradd G. Burkhart, M.D., presents "Lower Extremity Tendinopathies in Sports" at the 2013 9th Annual Cutting Edge Concepts in Orthopaedics & Sports Medicine Seminar presented by Orlando Orthopaedic
Bradd G. Burkhart, M.D., presents "Lower Extremity Tendinopathies in Sports" at the 2013 9th Annual Cutting Edge Concepts in Orthopaedics & Sports Medicine Seminar presented by Orlando Orthopaedic Center Foundation.
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!)
7. Tendon-bone junction• Dense tendon• Fibrocartilage• Mineralized fibrocartilage• Bone
8. 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
9. Biomechanics• Tendons are highly flexible, elastic and mechanically strong• They are viscoelastic and therefore follow the stress/strain curve we all know and love!
10. Pathology• Rupture• Tendinopathy
11. 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
12. 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
13. 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)
14. • 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
15. 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
16. 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!
17. 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
18. • 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?
19. 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
21. 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
22. 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
23. 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
24. Achilles• Conservative treatment initially• NSAIDs, rest, stretching• Immobilization if needed• All else fails? MRI to examine extent of involvement, possible surgical reconstruction
25. 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
26. 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.