Soft Tissue Healing

Introduction

After an injury, the soft tissue structures in the body undergo a natural healing process of specific healing stages.

• The timeline for healing depends on: the individual; the extent of the injury; age; and overall health.
• Physiotherapy helps promote healthier healing – thereby reducing the risk of re-injury chronic pain and functional impairment.
• One of the main risks of future injury is how the soft tissue recovers or recovers from previous injuries/surgeries.

Soft tissue healing is defined as the replacement of damaged tissue by living tissue in vivo. [1] This process consists of two parts – regeneration and repair. [2] Note – as the wound healing response “transitions” to the next phase, there are no clear boundaries between phases Healing [3].

• During regeneration, specialized tissue is replaced by proliferation of surrounding undamaged specialized cells.
• In the repair component, lost tissue is replaced by granulation tissue, which matures into scar tissue. [2]

The cellular response to injury depends on the type of tissue and the extent of the wound.

• In CNS tissue injury, which damages both neurons and supporting glial cells, the body’s response is relentless because it is impossible for lost neurons to regenerate. Activated astrocytes insulate the lesion, forming a glial scar.
• In contrast, in non-CNS tissues, a single tissue type can produce multiple responses depending on the degree of injury. [3]

Phases of Healing

The different healing stages are not mutually exclusive, and there is often a lot of overlap. [2]

Bleeding Phase

Transient phase after injury – lasts approximately 6-8 hours, up to 24 hours after a crush injury.

• Bleeding time depends on the extent of soft tissue injury and its management.
• The more blood vessels an injured structure has, the more it will bleed. [2]

Inflammation Phase

The goal of the inflammatory phase is the hemostatic phase.

• This phase begins rapidly within 6-8 hours after the soft tissue injury reaches its maximum response within 1-3 days and gradually resolves over several weeks. [2]
• Fibrin deposition and coagulation is achieved by vasoconstriction constricting damaged blood vessels.
• The blood supply to the area increases at this time, causing edema and redness.
• Phagocytosis (phagocytosis and usually destruction of particulate matter by phagocytic cells, an important body defense mechanism against microbial infection and clogging of mucus surfaces or tissues with foreign particles and tissue debris [4]) occurs during stage 2]

1. The acute inflammatory response involves activity that produces an exudate – a plasma-like fluid that seeps from tissue or its capillaries, consisting of protein and granular leukocytes (leukocytes). [5]
2. The chronic inflammatory response is longer lasting and involves the presence of nongranular leukocytes and the production of scar tissue.

The acute phase involves three mechanisms that prevent blood loss from the wound:[5]

1. Local vasoconstriction lasts from a few seconds to up to 10 minutes. Larger blood vessels constrict due to neurotransmitters and capillaries, and smaller arterioles and venules constrict due to the influence of serotonin and catecholamines released from platelets. The resulting reduction Blood flow to the area increases blood viscosity, or resistance to blood flow, which further reduces blood loss from the injured area.
2. The platelet response triggers coagulation as individual cells irreversibly bind to each other and to fibrin to form a mechanical plug that plugs the ends of ruptured blood vessels. Platelets also produce a series of chemical mediators during the inflammatory phase: serotonin epinephrine Norepinephrine and histamine. ATP is also used to provide energy during the healing process.
3. The fibrinogen molecule is converted to fibrin to form the clot.

Swelling, or edema, occurs approximately 1 hour after injury as vessel walls become more permeable and increased intravascular pressure forces plasma to leak out into the interstitium. This happens at:

• Minor trauma – lasts a few minutes, permeability returns to normal after 20-30 minutes. [5]
• More severe trauma – a long-term condition that may result in increased permeability, sometimes delayed onset of increased permeability, swelling not evident until some time has elapsed since the initial injury.

Bradykinin, a major plasma protease present during inflammation, increases vascular permeability and stimulates nerve endings to cause pain [5].

Proliferation Phase

This phase begins 24-48 hours after the injury and lasts 2-3 weeks when most of the scar tissue has formed. [2]

Fibroplasia and granulation tissue formation

• Central event of the proliferative phase.
• Occurs 3-5 days after injury and overlaps with the previous inflammatory phase.
• Granulation tissue includes inflammatory cells, fibroblasts, and neovasculature in a matrix of fibronectin, collagen, glycosaminoglycans, and proteoglycans. [6]

Epithelialization

Epithelium forms on exposed surfaces. This process begins within hours of tissue damage.

• Cells involved in the wound margin migrated less than 1 mm from one side of the incision to the other. Incisional wounds epithelialize within 24-48 hours of injury. This epithelial layer provides a seal between the underlying wound and the environment. [6]
• Epidermal cells at the wound margin undergo structural changes that cause them to lose their connections with other epidermal cells and the basement membrane. The formation of intracellular actin filaments allows epidermal cells to crawl across the wound surface.
• Application of occlusive and semi-occlusive dressings during the first 48 hours after injury maintains tissue moisture and optimizes epithelialization. [6]
• After epithelialization is complete, epidermal cells assume their original morphology [6]

Fibroplasia

Fibrous hyperplasia begins 3-5 days after injury and can last up to 14 days.

• Skin fibroblasts and mesenchymal cells differentiate to perform migratory and contractile abilities.
• Fibroblasts are responsible for the production of collagen, elastin, fibronectin, glycosaminoglycans and proteases.
• As the number of inflammatory cells decreases, fibroblasts fill in the gaps left by the open wound. [6]
• As the granulation tissue matures, fibroblasts produce less type III collagen and become more elongated in appearance. They start producing stronger type I collagen

Angiogenesis

Angiogenesis results in more blood flow to the wound, thus increasing the perfusion of healing factors. As the demand for new blood vessels ceases, so does angiogenesis. New blood vessels that are no longer needed disappear through apoptosis. [6]

• A rich blood supply is essential to maintain newly formed tissue (as evidenced by newly scarred erythema).
• Macrophages are critical for stimulating angiogenesis and produce macrophage-derived angiogenic factors in response to low tissue oxygenation. [6]

Contraction

• Contraction results in a reduction in wound size, eg a 2 cm incision may measure 1.8 cm after contraction.
• Loose tissue contracts more than less lax tissue, and square wounds contract more than round wounds.
• Wound contraction depends on the attachment of myofibroblasts located around the wound to extracellular matrix components and the proliferation of myofibroblasts. [6]
• Radiation and drugs that inhibit cell division have been noted to delay wound contraction.

Remodelling Phase

This phase begins at the peak of the proliferative phase. The result of this stage is an organized mass and functional scar that resembles the tissue it is busy repairing. [2]

The final endpoint after remodeling depends on the tissue type.

• Non-central nervous system (CNS) tissues undergoing primary healing undergo little remodeling due to the lack of extracellular matrix produced during repair. In contrast, secondary healing involves fiber alignment and contraction to reduce wound size and rebuild tissue strength. Full restoration of original tissue strength is rarely achieved in secondary healing because repaired tissue is less organized than uninjured tissue, which can lead to scarring. [6] Collagen-rich scars are morphologically characterized by a lack of specific tissue Cellular and matrix elements that make up the surrounding uninjured tissue.
• CNS Tissue – Damaged neurons are not repaired or regenerated, and there is relatively little re-establishment of the structural integrity of the region. During CNS remodeling, activated astrocytes insulate lesions and form glial scars. These activated astrocytes protect against further tissue damage, although Neuronal axon regeneration is inhibited. [3] [6]

Types

Primary Intention

Restoration of continuity occurs directly through fibroadhesion, without granulation tissue formation; it causes scar thinning. [7]

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Secondary Intention

Wound healing occurs through adhesive bonding of granulation surfaces when the edges of the wound are far apart and cannot come together. Granulation forms from the bottom and sides of the wound towards the surface. [7]

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Tertiary Intention

Wound healing occurs by progressive filling of the wound cavity with granulation and scarring. [7]

Physiotherapy Management

This classification is based on the treatment regimen of Clanton et al. [8] but it is similar to other classifications. Depending on the individual’s response to healing and the type of injury, some stages may overlap. Not every patient goes through all stages to achieve full recovery.

Phase 1: Acute Phase (1 – 7 Days)

• Goal: Minimize inflammation and pain.
• Treatment:
  • RICE Method: Resting Ice Compression and Elevation
  • Cryotherapy Pain Free Range of Motion

Phase 2: Subacute phase (Day 3 – < 3 weeks)

This phase begins when signs of inflammation begin to diminish. Signs of inflammation are hot swelling, redness and pain.

• Goal: Prevent muscle atrophy
• Treatment:
  • Painless Full Range of Motion: Concentric Strengthening
  • If any pain occurs: reduce exercise intensity

Phase 3: Reshaping Phase: (1 – 6 weeks)

• Stretch to avoid loss of flexibility
• Eccentric strengthening
• It is important to ensure that the muscle has regenerated to prevent the risk of re-injury

Stage 4: Functional Stage: (2 weeks – 6 months)

• Goal: Return to sport without re-injury.
• Treatment:
  • Increase their strength endurance speed agility flexibility and proprioception
  • Sport-specific activities

Phase 5: Return to Play Phase: (3 weeks to 6 months)

• Goal: Avoid a re-injury
• Standard: Full range of movement intensity coordination and mental preparation
• Treatment:
  • Address deficits in criteria
  • Progressive agility and trunk stability [9]

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Clinical Bottom Line

Soft tissue healing is a natural process that occurs after an injury to the body. This process occurs without medication and therapy, but can play an important role in cases where problems are identified in this natural process, such as repeated trauma-inhibited or delayed responses reaction. The goal will be to facilitate and stimulate the soft tissue healing process. [2] It is also important to recognize that inappropriate treatment can suppress these events. Therefore, it is very important to choose the most appropriate treatment at each stage.