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Soft Tissue Injury

Soft tissue injury of all types is extremely common in the general population. This injury can be classified as primary or secondary tissue injury.

Studies have shown that there is a linear relationship between soft tissue injury and aging, with fewer than 10% of individuals younger than 34 years being affected, in contrast to 32–49% of those older than 75 being affected.

Whether a stress proves to be beneficial or detrimental to a tissue is very much dependent on the physiologic capacity of the tissue to accept load.

The physiologic capacity of the tissue is dependent on a number of factors, among them:

Health of the tissue: Healthy tissues are able to resist changes in their shape. Any tissue weakened by disease or trauma may not be able to adequately resist the application of force.

Age: Increasing age reduces the capacity of the tissues to cope with stress loading.

Proteoglycan and collagen content of the tissue: Both increasing age and exposure to trauma can result in unfavorable alterations in the proteoglycan and collagen content of the tissue.

Ability of the tissue to undergo adaptive change: All musculoskeletal tissue has the capacity to adapt to change. This capacity to change is determined primarily by the viscoelastic property of the tissue.

The speed at which the adaptive change occurs: This is dependent on the type and severity of the insult to the tissue. Insults of low force and longer duration may provide the tissue an opportunity to adapt. In contrast, insults of a higher force and shorter duration are less likely to provide the tissue time to adapt.

The distinction between sudden and repetitive stress is important:

  • An acute stress (loading) occurs when a single force is large enough to cause injury on biological tissues; the causative force is termed macrotrauma.
  • A repetitive stress (loading) occurs when a single force itself is insufficient to cause injury on biological tissues. However, when repeated or chronic stress over a period of time causes an injury, the injury is called a chronic injury, and the causative mechanism is termed microtrauma.

Etiologic factors for microtraumatic soft tissue injury are of two basic types:

Intrinsic factors: are physical characteristics that predispose an individual to microtrauma injuries and include muscle imbalances, leg length discrepancies, and anatomical anomalies.

Extrinsic factors: which are the most common cause of microtrauma injuries, are related to the external conditions under which the activity is performed. These include training errors, type of terrain, environmental temperature, and incorrect use of equipment.

Soft Tissue Injury Classification

Soft tissue injury can be classified as primary or secondary tissue injury.

Primary Soft Tissue Injury:

Primary or macrotraumatic injuries can be self-inflicted, caused by another individual or entity, or caused by the environment. These injuries include fractures and dislocations, which are outside the scope of practice for a physical therapist, and subluxations, sprains, and strains, which make up the majority of conditions seen in the physical therapy clinic. For the purposes on the intervention, primary injuries are generally classified into acute, subacute, or chronic.

Acute: This type of Soft Tissue Injury is usually caused by macrotrauma and indicates the early phase of injury and healing, which typically lasts approximately 7–10 days.

Subacute: This phase occurs after the acute phase and typically lasts from 5–10 days after the acute phase has ended.

Chronic: This type of injury can have several definitions. On the one hand it may indicate the final stage of tissue healing that occurs 26–34 days after injury. On the other hand the term may be applied to an injury that lasts longer than normal and does not appear to be improving due to a persistent inflammatory state.

The persistent inflammatory state results in an accumulation of repetitive scar adhesions, degenerative changes, and other harmful effects referred to as subclinical adaptations.

Secondary Soft Tissue Injury:

Secondary or microtraumatic injuries are essentially the inflammatory response that occurs with the primary injury. Microtraumatic injuries include tendinitis, tenosynovitis, and bursitis.

Soft Tissue Injury types
Soft Tissue Injury types

Soft Tissue Healing

Fortunately, the majority of Soft Tissue Injury heal without complication in a predictable series of events.

The most important factor regulating the regional time line of healing is sufficient blood flow.

Complications such as infection, compromised circulation, and neuropathy have an adverse effect on the healing process and can cause great physical and psychological stress to the involved patients and their families.

Soft Tissue Healing
Soft Tissue Injury Healing

Tissue Healing Stages

After microtrauma, macrotrauma, or disease, the body attempts to heal itself through a predictable series of overlapping events that include coagulation and inflammation (acute), which begins shortly after the initial injury; a migratory and proliferative process (subacute), which begins within days and includes the major processes of healing; and a remodeling process (chronic), which may last for up to a year depending on the tissue type and is responsible for scar tissue formation and the development of new tissue.

Whereas simplification of the complex events of healing into separate categories may facilitate understanding of the phenomenon, in reality these events occur as an amalgamation of different reactions, both spatially and temporally.

Tissue Healing Stages
Soft Tissue Healing Stages

1. Coagulation and Inflammation Stage:

A soft tissue injury triggers a process that represents the body’s immediate reaction to trauma. The reaction that occurs immediately after a soft tissue injury includes a series of repair and defensive events. Following an injury to the tissues, the cellular and plasma components of blood and lymph enter the wound. Capillary blood flow is disrupted, causing hypoxia to the area. The blood congeals and, through several steps, a clot is formed. This initial period of vasoconstriction, which lasts 5–10 minutes, prompts a period of vasodilation, and the extravasation of blood constituents.

Extravasated blood contains platelets, which secrete substances that form a clot to prevent bleeding and infection, clean dead tissue and nourish white cells. These substances include macrophages and fibroblasts. Coagulation and platelet release results in the excretion of platelet-derived growth factor (PDGF), platelet factor transforming growth factor-alpha (TGF-a), and transforming growth factor-beta (TGF-b).

The main functions of a cell-rich tissue exudate are to provide cells capable of producing the components and biological mediators necessary for the directed reconstruction of damaged tissue while diluting microbial toxins and removing contaminants present in the wound. Inflammation is mediated by chemotactic substances, including anaphylatoxins that attract neutrophils and monocytes.

Neutrophils: Neutrophils are white blood cells of the polymorphonuclear (PMN) leukocyte subgroup (the others being eosinophils, and basophils) that are filled with granules of toxic chemicals (phagocytes) that enable them to bind to microorganisms, internalize them, and kill them.

Monocytes: Monocytes are white blood cells of the mononuclear leukocyte subgroup (the other being lymphocytes). The monocytes migrate into tissues and develop into macrophages, providing immunological defenses against many infectious organisms. Macrophages serve to orchestrate a long term response to injured cells subsequent to the acute response.

Neutrophils & Monocytes
Neutrophils & Monocytes

The white blood cells of the inflammatory stage serve to clean the wound debris of foreign substances, increase vascular permeability, and promote fibroblast activity. Other cell participants include local immune accessory cells, such as endothelial cells, mast cells, and tissue fibroblasts. The PMN leukocytes, through their characteristic “respiratory burst” activity, produce superoxide anion radical, which is well known to be critical for defense against bacteria and other pathogens. Superoxide is rapidly converted to a membrane permeable form, hydrogen peroxide (H2O2), by superoxide dismutase activity or even spontaneously.

Release of H2O2 may promote formation of other oxidants that are more stable (longer half-life) including hypochlorous acid, chloramines, and aldehydes. The phagocytic cells that initiate the innate immune response produce a set of proinflammatory cytokines (e.g., TNF-a, IL-1, and IL-6) in the form of a cascade that amplifies the local inflammatory response, influences the adaptive immune response, and serves to signal the CNS of an inflammatory response.

The extent and severity of this inflammatory response depend on the size and the type of the injury, the tissue involved, and the vascularity of that tissue.

Local vasodilation is promoted by biologically active products of the complement and kinin cascades:

  • The complement cascade involves 20 or more proteins that circulate throughout the blood in an inactive form. After soft tissue injury, activation of the complement cascade produces a variety of proteins with activities essential to healing.
  • The kinin cascade is responsible for the transformation of the inactive enzyme kallikrein, which is present in both blood and tissue, to its active form, bradykinin. Bradykinin also contributes to the production of tissue exudate through the promotion of vasodilation and increased vessel-wall permeability.

Because of the variety of vascular and other physiological responses occurring, this stage of soft tissue healing is characterized by:

  1. swelling,
  2. redness,
  3. heat,
  4. impairment or loss of function.

The edema is due to an increase in the permeability of the venules, plasma proteins, and leukocytes, which leak into the site of injury, resulting in edema. New stroma, often called granulation tissue, begins to invade the wound space approximately 4 days after injury. The complete removal of the wound debris marks the end of the inflammatory process.

Clinically, this stage is characterized by pain at rest or with active motion, or when specific stress is applied to the injured structure. The pain, if severe enough, can result in muscle guarding and a loss of function.

Two key types of inflammation are recognized: the normal acute inflammatory response and an abnormal, chronic, or
persistent inflammatory response.

Common causes for a persistent chronic inflammatory response include:

  1. infectious agents,
  2. persistent viruses,
  3. hypertrophic scarring,
  4. poor blood supply,
  5. edema,
  6. repetitive mechanical trauma,
  7. excessive tension at the wound site,
  8. hypersensitivity reactions.

The monocyte-predominant infiltration, angiogenesis, and fibrous change are the most characteristic morphologic features of chronic inflammation. This perpetuation of inflammation involves the binding of neutrophilic myeloperoxidase to the macrophage mannose receptor.

2. Migratory and Proliferative Stage:

The second stage of soft tissue healing, characterized by migration and proliferation, usually occurs from the time of the initial injury and overlaps the inflammation phase. This stage is responsible for the development of wound tensile strength.

Characteristic changes include:

  1. capillary growth
  2. granulation tissue formation,
  3. fibroblast proliferation with collagen synthesis,
  4. increased macrophage and mast cell activity.

After the wound base is free of necrotic tissue, the body begins to work to close the wound.

The connective tissue in healing wounds is composed primarily of:

  1. collagen, types I and III,
  2. cells,
  3. vessels,
  4. a matrix that contains glycoproteins and proteoglycans.

Proliferation of collagen results from the actions of the fibroblasts that have been attracted to the area and stimulated to multiply by growth factors, such as PDGF, TGF-b, fibroblast growth factor (FGF), epidermal growth factor, and insulin-like growth factor-1, and tissue factors such as fibronectin. This proliferation produces first fibrinogen and then fibrin, which eventually becomes organized into a honeycomb matrix and walls off the injured site.

The wound matrix functions as a glue to hold the wound edges together, giving it some mechanical protection while also preventing the spread of infection. However, the wound matrix has a low tensile strength and is vulnerable to breakdown until the provisional extracellular matrix (ECM) is replaced with a collagenous matrix. The collagenous matrix facilitates angiogenesis by providing time and protection to new and friable vessels. Angiogenesis occurs in response to the hypoxic state created by tissue damage as well as to factors released from cells during injury.

The process of neovascularization during this phase provides a granular appearance to the wound as a result of the formation of loops of capillaries and migration of macrophages, fibroblasts, and endothelial cells into the wound matrix.

Once an abundant collagen matrix has been deposited in the wound, the fibroblasts stop producing collagen, and the fibroblast-rich granulation tissue is replaced by a relatively acellular scar, marking the end of this stage.

This fibrous tissue repair process occurs gradually and can last anywhere from 5 to 15 days to approximately 10 weeks, depending on the type of tissue and the extent of damage. Upon progressing to this stage, the active effusion and local erythema of the inflammation stage are no longer present clinically. However, residual effusion may still be present at this time and resist resorption.

3. Remodeling Stage:

An optimal wound environment lessens the duration of the inflammatory and proliferative phases and protects fragile tissue from breakdown during early remodeling. The remodeling phase involves a conversion of the initial healing tissue to scar tissue. This lengthy phase of contraction, tissue remodeling, and increasing tensile strength in the wound can last for up to 1 year.

Fibroblasts are responsible for the synthesis, deposition, and remodeling of the ECM. Following the deposition of granulation tissue, some fibroblasts are transformed into myofibroblasts, which congregate at the wound margins and start pulling the edges inward, reducing the size of the wound.

Increases in collagen types I and III and other aspects of the remodeling process are responsible for wound contraction and visible scar formation. Epithelial cells migrate from the wound edges and continue to migrate until similar cells from the opposite side are met. This contracted tissue, or scar tissue, is functionally inferior to original tissue and is a barrier to diffused oxygen and nutrients. Eventually, the new epidermis becomes toughened by the production of the protein keratin. The visible scar changes color from red or purple that blanches with slight pressure to non-blanchable white as the scar matures.

Imbalances in collagen synthesis and degradation during this phase of healing may result in hypertrophic scarring or keloid formation with superficial wounds. If the healing tissues are kept immobile, the fibrous repair is weak and there are no forces influencing the collagen if left untreated, the scar formed is less than 20% of its original size.

Contraction of the scar results from cross-linking of the collagen fibers and bundles, and adhesions between the immature collagen and surrounding tissues, producing hypomobility. In areas where the skin is loose and mobile, this creates minimal effect. However, in areas such as the dorsum of the hand where there is no extra skin, wound contracture can have a significant effect on function. Consequently, controlled stresses must always be applied to new scar tissue to help prevent it from shortening. Scarring that occurs parallel to the line of force of a structure is less vulnerable to reinjury than a scar that is perpendicular to those lines of force.

Normally, the remodeling phase is characterized by a progression to pain-free function and activity. Clinically, the chronic inflammatory response is characterized by the signs and symptoms of acute inflammation (redness, heat, edema, and pain), but at a much less pronounced level.

hypertrophic scarring
Hypertrophic Scarring

Factors Affecting Wound Healing

Many factors can determine the outcome of the soft tissue injury:

Intrinsic (Local) Factors:

  • Extent of injury: Microtears involve only minor damage, whereas macro tears involve significantly greater destruction.
  • Edema: Swelling can cause increased pressure that can impede nutrition to the injured part, inhibit neuromuscular control, and retard the healing process.
  • Hemorrhage: Bleeding produces the same negative effects on healing as does the accumulation of edema.
  • Poor vascular supply: Wounds heal poorly and at a slower rate when the blood supply is inadequate.
  • Separation of tissue: A wound that has smooth edges and good apposition will tend to heal by primary intention with minimal scarring.
  • Muscle spasm: Spasm causes traction on the already torn tissue, preventing approximation.
  • Atrophy: Considered a secondary impairment to injury and subsequent disuse.
  • Degree of scarring: Scarring that occurs normally, but hypertrophic scarring produces keloids when the rate of collagen production exceeds the rate of collagen breakdown.

Systemic Factors:

  • Age: The ability to heal injuries decreases with age.
  • Obesity: Oxygen pressure in the tissues is lower in obese patients.
  • Malnutrition: Wound healing places a higher than usual demand on a patient’s energy resources. In every stage of wound healing, protein is needed. In addition adequate nutritional intake and body stores of all vitamins are essential.
  • Hormone levels: Hormones affect the composition and structure of a variety of tissues.
  • Infection: Infection can delay healing.
  • General health: Comorbidity can play a significant role in the overall healing process. For example diabetes can impede tissue healing.

Extrinsic Factors:

  • Drugs: Nonsteroidal anti-inflammatory drugs and corticosteroids decrease inflammation and swelling, resulting in decreased pain.
  • Absorbent dressings: The degree of humidity greatly affects the process of epithelialization, the epithelium regenerates twice as quickly in a moist environment
  • Temperature, and oxygen tension: Hypothermia has a negative effect on healing. Oxygen tension relates to the neovascularization of the wound.
  • Physical modalities: These can be used to promote an efficient healing environment for an injury when used individually, or in combination with other modalities or exercise.
  • Exercise: Exercise can help in the remodeling process of all connective tissues. Wolff’s law states that tissue remodeling and the response to therapeutic exercise are determined by the specific adaptation of the tissue to the imposed level of demand.

The focus of the rehabilitation should be to improve an individual’s range of motion, flexibility, strength, and coordination to a level that approximate the demands of the desired activity (speed, agility, strength, power, endurance.)


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