TISSUE INJURY & HEALING RATES

Tissue Injury and Healing Rates

by Alex Blacke (Chiropractor)

 A common question we encounter at KC The Sports Chiropractor for obvious reasons is

“how long will this take to recover/heal?”

This is a tricky question for a few reasons as it depends on:

○      The severity of the injury

○      Whether it is an acute or chronic injury

○      Age

○      Stress and anxiety

○      Underlying conditions that you might have (eg; diabetes, immunosuppressed states such as cancer etc)

○      Medications/drugs

○      Smoking status

If you compare two people with the exact same injury - they are not going to have the exact same healing rates/rate of recovery because they will have a different combination of the above factors.

______________________________________________________________________

Basic Processes of Wound Healing

Wound healing can be roughly divided into three overlapping phases following bleeding. This includes an inflammatory phase, a tissue proliferative phase and a tissue remodelling phase.

Inflammatory Phase

●      Can be subdivided into vascular and cellular responses

●      Local vasodilation (blood vessels widen) occurs

●      Blood and fluids leak outside the blood vessels into the tissues of the injured area

○      Blocks any lymphatic drainage producing typical signs of inflammation (redness, swelling and heat)

●      This acute inflammatory reaction lasts for 24-48 hours and can persist for up to two weeks

●      Tissue injury causes damage to the blood vessels and therefore bleeding

○      This causes platelets to coagulate and form a clot

○      They also release chemicals that initiate the healing response

●      Special white blood cells called neutrophils and macrophages move into the wounded area and assist in cleaning up and removing damaged tissue and foreign debris

●      Macrophages release some chemicals that initiate growth of tissue

 

Proliferative Phase

●      The previous phase provides the necessary scaffolding for tissues to start to regenerate

●      Major events in this phase include creation of a permeable barrier, establishment of blood supply and reinforcement of injured tissue

●      There is an increase in production of special cells called keratinocytes which migrate from the outer edges of the wound toward the centre and provide an adequate supply of cells to start covering the injury

●      As inflammatory cell numbers decrease, fibroblast cells start to grow in the wound

●      Fibroblasts are important cells for the formation of granulation tissue and are responsible for production of various important substances such as collagen, elastin and more.

●      This process is called ‘fibroplasia’ and begins 3-5 days after injury and continues for around 2 weeks.

●      Angiogenesis is the production of a new blood supply to the area. This leads to greater blood flow to the wound and an influx of important healing molecules and chemicals.

●      Contraction is the process of decreasing the size of the wound and it depends on wound shape, depth and tissue flexibility. Myofibroblasts predominate in this process because of their ability to extend and retract.

●      Myofibroblasts contain one of the highest concentrations of actinomyosin of any cell. The cells within the wound align along the lines of contraction and contraction of the wound occurs in directions of skin tension lines.

●      Myofibroblast pseudopodia extend, and cytoplasmic actin binds to extracellular fibronectin, attaches to the collagen fibres, and retracts, drawing the collagen fibres to the cell thereby producing wound contraction.

 

Maturation and Remodelling

 ●      Remodelling occurs throughout the entire wound repair process

●      The fibrin clot formed in the inflammatory phase is replaced with granulation tissue (consisting of type 3 collagen and blood vessels) in the proliferative phase, which is then replaced by a collagenous scar predominantly made of type 1 collagen.

●      For a period of one year or longer, the wound gradually returns to a stable pre-injury state, consisting mostly of type 1 collagen

●      There is a gradual turnover of collagen as type 3 collagen gets broken down and type 1 collagen production increases

●      The biomechanical stress and strain endured by the closed wound allows for this conversion of collagen

●      At 1 month of healing, the tensile strength of collagen is around 40% of its original strength pre-injury and at 1 year it reaches 70%.

______________________________________________________________________

Factors That Hinder the Above Processes

As stated earlier, no two people who have the same injury are going to heal at exactly the same rate for various reasons. Below is a table listing complicating factors for tissue healing rates and how they affect healing.

Complicating Factor: Severity of injury

How it can impact healing: Obviously, a full tear of a certain tissue (ligament, tendon, muscle etc) is going to heal slower than a mild grade 1 tear

Complicating Factor: Acute or chronic injury

How it can impact healing: Acute wounds usually go through the overlapping events listed above, healing-impaired chronic wounds do not progress normally through this sequence. Different areas of the wound can be found in different phases. Some of the cells involved in the normal healing process have been found to be unresponsive to activation signals.

Complicating Factor: Age

How it can impact healing: People who are over 60 tend to display changes in the normal wound healing process. In each phase of the healing process there appears to be a reduction in secretion of growth factors, impaired macrophage function, delayed angiogenesis, decreased wound strength and more.

Complicating Factor: Stress and anxiety

How it can impact healing: Stress increases production of glucocorticoids which reduces the level of pro-inflammatory chemicals at the wound site which are necessary for the first phase of healing. Glucocorticoids also suppress differentiation and proliferation of immune cells which are essential in the first phase of healing.

Stress and anxiety can also effect wound healing by leading to unhealthy habits such as poor sleep habits, lack of exercise and inadequate nutrition. People who are stressed about their injury may engage in ‘fear-avoidance’ behaviour where they are too scared to engage exercise which is necessary for tissues to learn how to deal with load.

Complicating Factor: Other medical conditions

How it can impact healing: People who are immunocompromised (weakened immune systems) display a decrease in healing rates. For example, people with diabetes tend to experience tissue hypoxia (oxygen deficiency), dysfunctional wound healing cells such as fibroblasts, impairment in growth of new blood vessels, decreased immune resistance and also damage to nerves (neuropathy) which can hinder their ability to detect tissue injury.

Complicating Factor: Drugs

How it can impact healing: Some drugs such as corticosteroids may be helpful short term to reduce pain and inflammation, however they have been found to suppress fibroblast proliferation and collagen synthesis. They also lower the immune system which can potentially lead to infections. There is also some evidence to suggest that NSAIDs (ibuprofen etc) can exhibit anti-proliferative effects.

Complicating Factor: Smoking

How it can impact healing: Various chemicals in cigarettes interfere with oxygen supply to the wound side. Nicotine has been found to induce vasoconstriction which therefore causes decreased tissue blood perfusion rates. Carbon monoxide in cigarettes also aggressively binds to haemoglobin with an affinity of 200 times greater than that of oxygen resulting in decreased oxygen in the blood stream.

______________________________________________________________________

References

1.     Enoch, S. and Leaper, D.J., 2008. Basic science of wound healing. Surgery (Oxford), 26(2), pp.31-37.

2.     Guo, S.A. and DiPietro, L.A., 2010. Factors affecting wound healing. Journal of dental research, 89(3), pp.219-229.

3.     Kim, B.C., Kim, H.T., Park, S.H., Cha, J.S., Yufit, T., Kim, S.J. and Falanga, V., 2003. Fibroblasts from chronic wounds show altered TGF‐β‐signaling and decreased TGF‐β Type II Receptor expression. Journal of cellular physiology, 195(3), pp.331-336.

4.     Li, J., Chen, J. and Kirsner, R., 2007. Pathophysiology of acute wound healing. Clinics in dermatology, 25(1), pp.9-18

5.     Stojadinovic, O., Brem, H., Vouthounis, C., Lee, B., Fallon, J., Stallcup, M., Merchant, A., Galiano, R.D. and Tomic-Canic, M., 2005. Molecular pathogenesis of chronic wounds: the role of β-catenin and c-myc in the inhibition of epithelialization and wound healing. The American journal of pathology, 1