
























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 -
The proliferative phase is essentially the generation of repair material which involves
the production of scar tissue (type III collagen), which commences after 2-
References:
1. Evans, P. (1980). The healing process at cellular level: a review. Physiotherapy,
66(8), 256-
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-
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-
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-
5. Watson, T. (2006). Tissue repair: the current state of art. Journal of Sportex
Health. 19, 8-
6. Glasgow, P. (2007). Sports rehabilitation: principles and practice. Journal
of Sportex Medicine. 32, 10-
7. Watson, T. (2003). Soft tissue healing. In Touch. 104, 2-
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-
10. Arem, A.J., Madden, J.W. (1976). Effects of stress on healing wounds: Intermittent
noncyclical tension. Journal of Surgical Research, 20 (2), 93-
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-
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-
13. Lederman, E. (2005). The science and practice of manual therapy. Second edition. Edinburgh: Churchill Livingstone.
.
Inflammation Phase -
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-
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-
Fig. 2. Hypothetical model of tissue tensile strength during healing
Adapted from: Hunter (1998). Specific soft tissue mobilisation etc.
Remodelling Phase:
Approximately 2-
BLEEDING
INFLAMMATION
PROLIFERATION
REMODELLING
