Today’s guest post is a real thought provoking piece on adhesions by Chris Lofquist. Interesting thoughts Chris, appreciate the contribution to the site and the nice article.
Adhesions
Let me start by saying this is by no means an exhaustive explanation of the pathology of adhesion or scar tissue, but a brief overview. When the phrase scar tissue is mentioned, most people think of external scarring or scars formed from surgery, when this is only a specific type of what could more generally be termed as adhesion formation. Scar tissue or adhesion is most commonly recognized as the fibrous connective tissue that is formed over a damaged area as the body attempts to repair this damaged tissue. The more commonly overlooked sources of adhesion, beyond acute injury, are microtrauma and hypoxia, which will also be discussed.
The Connective Tissue Healing Process
The healing process in connective tissue has four components, the formation of new blood vessels, the migration and proliferation of fibroblasts, the deposition of extracellular matrix and the maturation and reorganization of fibrous (scar) tissue. This last step, the remodeling process, when left on its own can take as little as 3 days, but typically takes 30 days to 2 years, and in some cases never truly reorganizes in a proper pattern.
Scar tissue or adhesions lead to a variety of symptoms such as:
- Reduced Range of Motion
- Muscle Weakness
- Pain
- Compensation patterns which cause problems in seemingly unrelated areas
- If a nerve is entrapped it can cause numbness, burning or tingling
Soft Tissue Dysfunction
Adhesion is one of the most common causes of soft tissue restriction, and the breakdown of adhesion appears to be a very feasible explanation behind how so many soft tissue treatment techniques work. When this adhesion is broken down, normal loading patterns are more easily established. When tissues are loaded in the manner in which they are designed and do not exceed their ability to recover, complete healing is allowed to take place.
Adhesion can form between any two surfaces within the body and can cause a decrease in global and segmental ranges of motion, as well as affect the speed and quality of those motions. These tests are not specific for adhesion, so a full assessment, including palpation to determine if adhesion is present and its specific location is required. This adhesion between two surfaces or within a structure itself can be a result hypoxia, microtrauma, or macrotrauma as mentioned before. Unfortunately we currently do not have reliable technology to run a diagnostic test for the presence of adhesion. This means detection relies on skilled palpation and having a keen eye for biomechanical dysfunction and compensation. Pain can be helpful, but as we all know, pain is a liar.
The Effect of Hypoxia
Hypoxia causes not only cell death, but also fibroblastic proliferation and free radical proliferation. Free radical proliferation then leads to the production of fibrous adhesion. Fibrous adhesion via fibroblastic activity is an often overlooked cause of musculoskeletal dysfunction. The reason this is often overlooked seems to be lack of exposure to the pathology itself. Simply put, a healthcare provider will never find a pathology they do not look for, or they don’t know exists. As a side note, Dr. William Brady has an excellent in depth description of this pathway at his blog.
Microtrauma induced scar tissue formation occurs in a similar pathway as macrotrauma, however if damage is continually induced in an area, collagen cannot remodel itself in an efficient pattern. With this repetitive damage there is also a risk of the myofibroblast rearing its ugly head in a chronic nature. The myofibroblast is a specialized contractile type of fibroblast. In normal situations, the myofibroblast allows for opposition of the separated areas in a damaged site, the myofibroblast exhibits contractile ability, allowing it to help close down this gap. After this gap has closed the myofibroblasts leave the area. If abnormal stresses are left in place without proper remodeling, the myofibroblast will remain active, inhibiting the normal range of motion in a tissue until these abnormal stresses are resolved. It is important that these abnormal stresses are addressed and soft tissue is permitted to remodel itself in conjunction with the surrounding tissue through manual therapy, stretching and exercises.
References
Special thanks to Dr. William Brady and Dr. Mike Leahy for helping me to understand these pathways and their implications.
- Kumar V & Ramzi Cotran. Robbins Basic Pathology 7th ed. Elsevier; pp 69-77.
- Falanga V, & Kirsner RS. Low oxygen stimulates proliferation of fibroblasts seeded as single cells. J of Cellular Physiology. 1993 Mar; 154(3):506-10.
- Leahy PM, Active Release Techniques: Soft Tissue Management System. 2nd Ed. 2008; pp 8-16.
- Hinz, B. The myofibroblast: paradigm for a mechanically active cell. J of Biomechanics 2010 Jan 5;43(1):146-55.
- Wipff, P & B Hinz, Myofibroblasts work best under stress. J of Bodywork & Movement Therapies 2009 Apr; 13(2):121-7.
Dr. Lofquist is a chiropractor and manual therapist practicing at Trenton Chiropractic & Rehab in Findlay, Ohio. He graduated with a Bachelor of Science in Athletic Training from Heidelberg University in Tiffin, OH and graduated from Logan University in St. Louis, MO with his Master of Science in Sport Science and Exercise Rehabilitation and his Doctorate in Chiropractic. He is a certified athletic trainer and is a consultant for several area collegiate athletic training departments.
