Soft Tissue Healing

A soft tissue injury is the damage of muscles, ligaments and tendons throughout the body when their tensile strength is interrupted. They normally result in pain, swelling and bruising as well as loss of function.

Tissue healing compromises two essential components: regeneration and repair (dependant on the resultant tissue). In regeneration specialised tissues is replaced by the proliferation of surrounding undamaged specialised cells. In repair, lost tissue is replaced by granulated tissue which matures to form scar tissue.

The healing process is divided into 4 phases: bleeding, inflammation, proliferation and remodelling. These 4 phases hugely overlap and integrate during repair.

Bleeding is a relatively short phase that occurs following trauma or another similar insult. The normal time for bleeding to stop varies depending on the injury and the tissue type. Vascular tissue such as muscle will bleed for longer causing a greater escape of blood into the surrounding tissues whereas other tissues such as a ligament will bleed less and for a shorter amount of time. The average bleeding time is 6-8 hours although is heavily dependent on the patient and the nature of the injury, for example a crush injury to a vascular tissue could continue bleeding, admittedly minimally, for 24 hours post trauma.

Inflammation is a normal and necessary prerequisite to healing (Hardy 1989) and onsets after a few hours. It rapidly increases in magnitude over the following 1-3 days before gradually resolving over the following couple of weeks. Signs of inflammation include: swelling, pain, redness, heat and loss of function.

The cascade that is responsible for the initiation and control of inflammation can be due to trauma, mechanical irritation, thermal or chemical insult as well as immune responses. Fibrin and fibronectin form a substratum (underlying foundation layer) which is hospitable to the adhesion of various cells. The two essential elements to inflammation are the vascular and cellular cascades. They occur in parallel and are somewhat interlinked.

Vascular events are additional to the initial bleeding. Vasodilation follows an initial brief vasoconstriction and there is an initial increase in the velocity of the blood followed by a prolonged slowing. The white cells form a margin, platelets adhere to the vessel walls and the endothelial cells (lining the blood vessels) swell. The local vessels also become more permeable, which when combined with vasodilation, increases the flow of blood through the more permeable vessels and results in exudate (including protein rich plasma) passing into the tissue spaces. This can be at both the arterial and venous ends of the capillary network as the increase hydrostatic pressure overcomes the osmotic pressure of the plasma proteins.

The effect of the exudate is to dilute any irritant substances in the damaged area and form a fibrin clot with the high fibrinogen content of the fluid. This union between the surrounding intact tissues forms a mesh which can trap foreign particles and debris. Mast cells in the damaged area release hyaluronic acid and other proteoglycans which bing with the exudate and create a gel which limits local fluid flow and further traps various particles and debris (Hardy 1989).

The cellular events of inflammation include the early emigration of the phagocytes within minutes. They are followed out of the vessels by monocytes, lymphocytes, eosinophils and basophils (Lorena et al 2002). Once in the tissue spaces monocytes become macrophages (Forrest 1983). These cells exhibit a strong phagocytic activity and are responsible for the removal of damaged tissue and foreign objects. And to top it all off lactic acid, one of the end products of phagocytosis, is a stimulant for proliferation. Pretty clever, ‘ey? Increased hydrostatic pressure for the oedema can be detrimental as it can restrict blood flow if the injured tissue space is limited, increasing pain and limiting function.

Proliferation is the generation and deposition of granulation (repair) tissue, which in the majority of musculoskeletal injuries is collagen (scar) material. It has a rapid onset of 24-48 hours but takes 2-3 weeks to reach its peak reactivity, although the more vascular the tissue the shorter the time taken to reach this peak phase. The bulk of the scar production is completed during this time, but proliferation decreases thereafter through several months post injury. The key events in proliferation are: fibroplasia (production of fibrous tissue), angiogenesis (development of blood capillaries), increased extracellular collagen production, wound contraction (from myofibroblasts) to minimise the scar and a complex interactive response amongst cells and chemical mediators to ensure effective completion of the scar tissue.

Remodelling is the strengthening (type I collagen replaces type III) and alignment of collagen that results in an organised, quality, functional scar that allows movement in a similar way to the original tissue. This phase is widely reported to begin at the same time as the peak of the proliferative phase (2-3 weeks) however further research shows that it may begin at around 1-2 weeks post injury. During this phase movement is essential to ensure that the collagen aligns in the direction most suited to functional activities. Signs of the remodelling phase include reduced redness, oedema and pain.

Factors that are known to delay healing can be general or local. General factors include age, protein deficiency, low vitamin C levels, steroids and NSAIDs as well as cold temperatures. Local factors include ischaemia, adhesion to bone of other underlying tissue, continued inflammation, drying of the wound and excessive movement as it restarts inflammation.