Introduction:

All connective tissue injuries, regardless of their severity, must undergo the same healing process (1,2,3). A consensus exists, consisting of 4 overlapping, interlinked phases (Fig.1); Bleeding, Inflammation, Proliferation, and Remodelling (4,5). It is generally accepted that treatment and rehabilitation should be based on sound scientific principles underlying tissue healing (2,6).

Figure 1.   The basic response to tissue injury

Adapted from: Watson, (2006). Tissue repair: the current state of art.

Proliferation Phase - Subacute:

The proliferative phase is essentially the generation of repair material which involves the production of scar tissue (type III collagen), which commences after 2-3 days, reaching a peak at 2-3 weeks post-injury. There are two fundamental processes involved; fibroplasia (formation of collagen) and angiogenesis (formation of new local blood vessels) (5). Although a short period of immobilization following injury is necessary (2,4), early controlled mobilisation is essential for decreased healing time, increased vascular ingrowth, quicker regeneration of scar tissue (10,11,12), resulting in stronger mobile tissue (6). Whereas, prolonged immobilization leads to deleterious tissue effects such as; random deposition of collagen, excessive cross-link formation and atrophy. Consequently this leads to functional implications such as losses in range of movement  and tensile strength (13).  

References:

1.   Evans, P. (1980). The healing process at cellular level: a review. Physiotherapy, 66(8), 256-259.

2.  Kannus, P., Parkkari, T.L., Jarvinen, T., et al. (2003). Basic science and clinical studies coincide: active treatment approach is needed after a sports injury. Scandinavian Journal of Medicine and Science in Sports. 13, 150-154.

3.   Vailas, A.C., Tipton, C.M., Matthes, R.D., Gart, M. (1981). Physical activity and its influence on the repair process of medial collateral ligaments. Connective Tissue Research, 9, 25-31.

4.  Jarvinen, M.J., Lehto, M.U. (1993). The effects of early mobilisation and immobilisation on the healing process following muscle injuries, Sports Medicine Journal, 15 (2), 78-89.

5.   Watson, T. (2006). Tissue repair: the current state of art. Journal of Sportex Health. 19, 8-12.

6.   Glasgow, P. (2007). Sports rehabilitation: principles and practice. Journal of Sportex Medicine. 32, 10-16.

7.   Watson, T. (2003). Soft tissue healing. In Touch. 104, 2-9.

8.   Underwood, J.C.E. (2000). General and systematic pathology. Third edition. Edinburgh: Churchill Livingstone.

9.   Hunter, G. (1998). Specific soft tissue mobilisation in the management of soft tissue dysfunction. Manual Therapy. 3(1), 2-11.

10. Arem, A.J., Madden, J.W. (1976). Effects of stress on healing wounds: Intermittent noncyclical tension.  Journal of Surgical Research, 20 (2), 93-102.

11. Buckwalter, J.A., Grodzinsky, A.J. (1999). Loading of healing bone, fibrous tissue, and muscle. Implications for orthopaedic practice. Journal of American Academic Orthopaedic Surgery. 7, 291-299.

12. Culav, E.M., Clark, C.H., Merrilees, M.J. (1999). Connective tissues: matrix composition and its relevance to physical therapy. Physical Therapy, 79(3), 308-319.

13. Lederman, E. (2005). The science and practice of manual therapy. Second edition. Edinburgh: Churchill Livingstone.

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Inflammation Phase - Acute:

Following injury, damaged blood vessels bleed causing hypoxia, so the injured tissue contains dead cells and extravasated blood (1). This triggers a natural but essential inflammatory reaction, involving a vascular and cellular response with fluid exudate, resulting in oedema and phagocytic activity (5). Acute inflammation results from vasodilatation and vasopermeability of the blood vessels, initiated and controlled by a wide array of chemical mediators released by the damaged tissues (7). Clinically, acute inflammation manifests as swelling, erythema, increased temperature, pain, leading to loss of function (2. The physical characteristics of acute inflammation were first formulated by Celsus in (30 BC – 38 AD) using Latin words; rubor, calor, tumor and dolor (8). Typically, the inflammatory phase (Lag phase) lasts between 4-6 days, and prepares the wound for the proliferation phase (9).

 Hours    Days         Weeks                                       Months

However, during early and intermediate subacute healing, new  tissue is fragile and easily interrupted, consequently, mobilisation too early or too intensively may re-rupture the injured tissue (2). Thus, exercise loading and intensity should remain within the tensile capability of the healing tissue (Fig. 2). Yet, careful tensioning of the healing tissue during the proliferation phase increases collagen synthesis, thus, potentially speeds up the healing process (9).

Fig. 2. Hypothetical model of tissue tensile strength during healing

Adapted from: Hunter (1998). Specific soft tissue mobilisation etc.

Remodelling Phase:

Approximately 2-3 weeks post-injury, collagen maturation and remodelling initiate (2,4). With maturity, the collagen remodels becoming more obviously oriented in line with local stresses (5). A portion of the type III collagen is reabsorbed and is replaced by type I collagen with greater tensile strength Remodelling continues for months, even years. The tensile strength of the tissue improves due to formation of intra and extra molecular cross linkages between the collagen fibres (9).

BLEEDING

INFLAMMATION

PROLIFERATION

REMODELLING