An evidence based approach to treating tendon problems.Introducing a new clinical model for diagnosis and management of muscolskeletal problems.By David Poulter PT
A Simple proposition:
Pain does not equal inflammation.There is a lot of evidence to suggest that 90% of what we thought was tendonitis is in fact tendonosis. The troubling aspect of this evidence is that 90% of patients presenting with tendon problems are receiving the wrong treatment. (12,16) Tendonosis is being treated as though it is an acute inflammatory condition. Current evidence suggests that most tendon problems lack an inflammatory mediator (prostaglandin E2). There is some discussion as to whether tendonitis is a precursor to tendonosis, but the current evidence leans towards the hypothesis that it is not.(2,16,17)
The literature also suggests that we have been treating everything as though it was inflamed. Recent studies have demonstrated that NSAIDS used in the early treatment of tendon problems are ineffective and may retard the healing process. There is evidence that used later in the condition they may be of some benefit.(9,10)
Simply put tendosis is a painful condition brought on by overloading connective tissue, which cannot keep pace with remodeling. There is no evidence of inflammatory cells in tissue samples; hence the condition does not follow a normal healing cycle. There is strong evidence of organized cell death “apoptosis” and increased tenocite activity, with disorganized collagen alignment. There is also strong evidence of neovascularization around the affected tendon.(2,3,7)
The literature suggests that neovascularization (new immature blood vessels) may be the cause of some of the pain, there has been work done by Alfredson and his group on sclerosing the vessels, which leads to athletes becoming pain free. These neovessels are also enriched with new nerves, which may also contribute to the pain.(4)
There is also strong evidence that the neurotransmitters Glutamate and Substance P have been found in high concentrations, in people with tendonosis, and a lack of prostaglandin E2. The relationship to pain production is still not clearly understood.(2,3,8,9)
Alfredson’s group in Sweden has done a lot of work on using eccentric loading to treat tendonosis, with good outcomes.(1,14,18) Purdham has also done work at the Australian Institute of Sport using incline eccentric squats for knee tendonosis with good results.(26) There is also strong evidence that eccentric programs have good effect on treating hip adductor problems, lateral elbow problems and shoulder tendonopahy.(14,19,12,26,27,28,29)
Current research also demonstrates good outcome from using Nitric oxide (glycerin trinitrate patches) in the treatment of tendonosis of the elbow, shoulder and Achilles.(20,23,24,25)
The Active/ Inactive model
I have propsoed a simple model known as the
Active /
Incative model for clinical reasoning. The model is based on the symptomatic and mechanical responses of patients to loading.
Definitions:
Mechanical Loading Strategy = Repeated movements, static
positions, functional tasks, manual techniques.
Active Condition = During the application of certain mechanical loading strategies there will be a change in the symptomatic presentation and / or the mechanical presentation, this change will remain on cessation of the loading strategy.
Inactive Condition = During the application of certain
mechanical loading strategies there may be a change in the symptomatic presentation and / or the mechanical presentation, but the change will never remain on cessation of the loading strategy.
The active/Inactive model is represented below in figure 1.
Figure 1. Poulter (c) 2008
The Active/Inactive model can be used to classify common musculoskeletal problems. This allows for simple treatment strategies to be carried out.
It can be seen that in the Active/Inactive model "Tendonosis" is classified as an Inactive pathalogical condition, which comes about as a result of Wolff's law. Wolff's law simply put states "Form follows Function". Tendonosis put in simple terms is the tissues failure to remodel succesfully to an external load being applied. The collagen disaray, cell apoptosis and glutimate presence are all refelctions of Wolff's law and the tissues failed adaptation to loading. (11, 12, 15)
We often give the beneficial effects of Wolff's law the label "Remodelled", the adverse effects are often given the label "Degenerated".
Good news: Even though Tendonosis is labelled as a degenerative condition it can be remodelled using the correct eccentric loading strategies. (1,2,3,4,5,,6,12,13)
The active/inactive model can be used to classify all common muskuloskeletal conditions, based on their symptomatic and mechanical responses to loading.
On the left side of the model I propose three ways that tissue can be damaged to lead to an active condition.
1. Over stressing tissue. Tissues have a stress strain curve which represents their response to external loading. Most tissues go through and elastic, to palstic, then failure phase. Over stressing tissue can lead to permenant deformation of the tissue, without necessarily breaking the tissue. If the tissue has an innervation this may case pain and micro fracturing of the tissue.
If the tissue doesn't have an innervation then it may displace (nucleus palposus), tear (labrum of hip or shoulder), or over stretch (inner annulus of disc) and lead to pain by placing stress on an innervated structure.
2. Inflammation. Inflammation can be casued by systemic auto immune disease such as Rheumatoid arthritis, Ankylosing Spondylitis, Psoriatic arthristis, Lupus, Reiters Disease, Stills Disease and other common arthitidese. It is well documented that these conditions go through active cycles and remissions.
3. Trauma. Simply put "tissue fracture". This leads to bleeding, clot formation and then the normal healing cycle. The first phase of trauma invovles inflammation caused by the tissue damage.
On the right hand side of the model there are three ways of returning to inactive.
1. Healing. There are recognised phase to the healing process. It is important to remember that each pahse is a predomination and that the other phses are taking place at a lower level all through the healing process.
Phases of Wound Healing
The entire wound healing process is a complex series of events that begins at the moment of injury and can continue for months to years. This overview will help in identifying the various stages of wound healing.
I. Inflammatory Phase
A) Immediate to 2-5 days
B) Hemostasis
Vasoconstriction
Platelet aggregation
Thromboplastin makes clot
C) Inflammation
Vasodilation
Phagocytosis
II. Proliferative Phase or Fibroplastic Phase.
A) 2 days to 3 weeks
B) Granulation
Fibroblasts lay bed of collagen
Fills defect and produces new capillaries
C) Contraction
Wound edges pull together to reduce defect
D) Epithelialization
Crosses moist surface
Cell travel about 3 cm from point of origin in all directions
III. Remodeling Phase
A) 3 weeks to 2 years
B) New collagen forms which increases tensile strength to wounds
C) Scar tissue is only 80 percent as strong as original tissue
2.Natural resolution: Natural resolution is different from healing becasue it does not go through a formal process of stages and does not take 6-12 weeks to show results functionally. Mytosis is a form of repair which can not be discribed in terms of healing, molecular reconstitution due to water reabsorption, hysteresis after tissue creep, realignment of tissue after stress are all examples of natrual resolution.
Non vascularized, non innervated tissues can not heal but they can under go remodeling and change their structure molecularly. They can also be affected by creep and hysteresis.
Resolution of pain and stiffness after a manipulation can not be described in terms of healing, but is a form of natural resolution.
3. Treatment: "Removal of the nasty things to provide an optimal environment for recovery."
Follows the D.Re.Ma.R concept of treatment. (Poulter 2008)
Diagnose, Reduce, Maintain, Restore Function
Classification using the active / inactive classification system
1. I.D.I.O.T.
Victims of creep also known as I.D.I.O.T. syndrome. Sustained loading with g
(gravity) over Time of normal tissue leads to
CREEP and the nociceptive system kicks in to warn of impending
damage to the tissue.
“I Do It Over Time”
This is superimposed on other problems.
This class is inactive non pathological
2. Mal-adaptation
This occurs as connective tissues (including scar) obey Wolff’s law. Generally this can be called other names such as degeneration, adaptive shortening, adhesions, “dysfunction”, instability from degenerative changes can also be included in this class.
The recent literature has also suggested that common tendon pathologies, and even muscular, capsular and ligamentous problems, are caused by an abortive remodeling process which cannot keep pace with the stress applied to them.
The pathology produces is Tendonosis.
Tendonosis is an inactive tendon pathology. ( Khan 2000, Cook 2000 )
Two ends of the spectrum of mal -adaptation are shortened scar or adhesion , restricting motion, or degenerative changes leading to abnormal excessive motion, often classed as instability, with tendonois changes in the middle.
Stable ………………Mal-adaptation………………unstable
(inactive pathological) (inactive pathological )
(Mechanical)
3. Re-arrangement
This class is defined by its active symptomatic and mechanical presentation. Hypothetically this is over stretching of the contents or supporting structures of a joint, leading to temporary or even permanent incongruity of the joint. It is often labeled as, subluxation, dislocation, instability, “derangement”, internal derangement.
Active pathological (mechanical primary, with possible secondary chemical)
4. Trauma
Simply put this involves tissue fracture, leading to a cascade of chemically mediated events, cardinal signs being, heat, redness, swelling and pain. (Calor, rubor, tumor, dalor). Trauma can range on a spectrum from mild to major, depending on the degree of damage and extent of the tissue damaged.
Active pathology (Mechanical leading to primary chemical, secondary mechanical from tissue swelling)
Mechanical Treatment Approach
I.D.I.O.T. (victim of creep): Avoidance of provocative postures and positions. Postural alteration, slouch overcorrect, regular interruption of sustained postures.
Mal-adaptation (with restrictive loss of function): “REMODEL.” Controlled return of stress / function using HURT not HARM principle. Understanding the patient is essential, it takes time to produce a restriction of function due to soft tissue changes and the patient is generally fearful and avoiding pain.
Note you cannot stretch mal-adapted tissue; it has to be remodeled over time. Patient generated forces are adequate to bring about remodeling over time if the appropriate functional stress is applied often enough.
Mal-adaptation (with instability): The treatment of mal-adaptation with excessive motion or instability is postural control and stability exercises (strengthening of postural control muscles). Neuromuscular re-education is often required to allow stability during function.
Mal-adaptation Tendonosis, ligosis, myosis, fasciosis.: The treatment of the “Osis”
is similar to remodeling the short contracted tissue form of mal-adapted tissue. The affected tissue needs loading in a gradual and repetitive fashion. “Eccentric loading”
allows us to apply load to the tenonosis to begin remodeling. In the case of myosis eccentric muscle work and often isometric muscle work allows remodeling to be achieved.
It is important to keep in mind the HURT not HARM system of applying load to the tissue.
Remodeling of and “osis” is a painful procedure and can take many months. Patient education and expectations should be addressed as part of the overall treatment strategy.
Rearrangement: The treatment of rearrangement follows the simple orthopedic principle of D.R.eM.aR.:
Diagnose, Reduce, Maintain & Restore Function. Patient self generated repeated movement to end range; static positions; patient forces and therapist forces are all used in the reductive stage. The P.O.O.M.M. Patient Centered Force Progression Model is followed.
(Over pressure can also be synergistic)Patient generated
Over pressure (Patient)
Over pressure (Therapist)
Mobilization
Manipulation.
Postures and positions are used in the maintenance stage.
Patient self generated repeated movements are used in the restoration of function stage.
Trauma (Tissue fracture): The treatment of trauma follows the D.R.eM.aR principle.
During the reduction phase the R.I.C.E. principle can be followed. (Rest, Ice, Compression, Elevation), in the first few days. Movement testing should begin as soon as possible, using the Hurt not Harm principle. A sign that movement is indicated is that the patients pain becomes intermittent.
Movement in the presence of healing is indicated as long as the symptomatic response to loading is monitored closely. Early controlled movement will give the message to the healing tissue to lay down in a functional orientation and prevent the development of mal-adaptation.
References:
1.Alfredson H et al: Heavy-Load Eccentric Calf Muscle Training For the Treatment of Chronic Achilles Tendinosis. THE AMERICAN JOURNAL OF SPORTS MEDICINE, Vol. 26, No. 3 1998
2.Alfredson H. In situ microdialysis in tendon tissue: high levels of glutamate,but not prostaglandin E2 in chronic achilles tendon pain. Knee Surg Sports Traumatol Arthrosc;7:378–81;1999.
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