High-yield map
Key points before the detail
- 01
The phases overlap; fixed start/stop times are approximations.
- 02
Macrophages are central coordinators of the transition from inflammation to repair.
- 03
The proliferative phase combines re-epithelialisation, granulation tissue, angiogenesis, fibroplasia and contraction.
- 04
Type III collagen is prominent early and is progressively replaced by a higher proportion of type I collagen during remodelling.
- 05
Healed skin gains strength over time but usually never recovers the full tensile strength of uninjured skin.
1. Four overlapping phases
| Phase | Approximate timing | Main participants | Main task |
|---|---|---|---|
| Haemostasis | Immediate to hours | Vasculature, platelets, coagulation | Limit bleeding and create a provisional fibrin matrix. |
| Inflammation | Hours to several days | Neutrophils, monocytes, macrophages | Control microbes/debris and coordinate repair. |
| Proliferation | Begins within days; continues for weeks | Keratinocytes, fibroblasts, endothelial cells, myofibroblasts | Re-epithelialisation, angiogenesis, matrix deposition and contraction. |
| Remodelling | Begins during proliferation; months or longer | Fibroblasts, myofibroblasts, MMPs and TIMPs | Collagen reorganisation, vascular regression and increasing tensile strength. |
2. Haemostasis: stop bleeding and build the provisional matrix
- Brief vasoconstriction reduces initial blood flow.
- von Willebrand factor links exposed subendothelial collagen to platelet GPIb; other collagen receptors contribute.
- Platelet activation releases mediators such as ADP and thromboxane A2; activated GPIIb/IIIa binds fibrinogen or vWF between platelets.
- Tissue factor promotes thrombin generation; thrombin converts fibrinogen to fibrin and factor XIII cross-links the clot.
- Activated platelets also release mediators including PDGF and TGF-beta that recruit inflammatory and stromal cells.
3. Inflammation: clear, signal and hand over
Neutrophils usually arrive early, especially when contamination or tissue damage is substantial. They phagocytose microbes and release antimicrobial products. Monocytes and macrophages become prominent over subsequent days, clear apoptotic cells and debris, and release mediators that drive angiogenesis, fibroblast activity and matrix deposition.
The familiar M1/M2 macrophage language is useful shorthand but oversimplifies a continuum of phenotypes. Clinically, the important point is that persistent necrosis, infection, foreign material or ischaemia can keep a wound trapped in a prolonged inflammatory state.
4. Proliferation: cover the surface and fill the defect
- Re-epithelialisation: keratinocytes migrate from wound edges and appendages, then proliferate to restore the barrier.
- Granulation tissue: new capillaries, fibroblasts, inflammatory cells and loose extracellular matrix create the red granular wound bed.
- Angiogenesis: hypoxia and mediators including VEGF stimulate endothelial sprouting and vessel maturation.
- Fibroplasia: fibroblasts deposit provisional matrix and collagen, initially rich in type III collagen.
- Contraction: myofibroblasts reduce wound area, particularly in wounds healing by secondary intention.
5. Remodelling: stronger does not mean “back to normal”
Remodelling begins before proliferation has finished and may continue for many months. Type III collagen is progressively replaced by a higher proportion of type I collagen, fibres align along mechanical stress and cross-linking increases. Excess vessels regress and cellularity falls, so the scar usually becomes flatter and paler.
Matrix metalloproteinases degrade extracellular matrix and TIMPs regulate them. Both excessive degradation and excessive deposition can become pathological. Tensile strength rises, but published percentages vary by tissue and method; healed skin usually does not regain the full strength of uninjured skin.
6. Growth factors worth knowing for MRCS
| Mediator | High-yield role |
|---|---|
| VEGF | Promotes angiogenesis and endothelial sprouting. |
| TGF-beta | Promotes fibroblast activity and collagen-rich matrix/scar formation while influencing matrix degradation. |
| PDGF | Recruits fibroblasts and macrophages and helps stabilise developing vessels. |
| FGF-2 | Supports proliferation of fibroblasts and endothelial cells among other repair effects. |
| EGF | Promotes epithelial proliferation and re-epithelialisation. |
7. Why wounds heal badly
Think mechanistically. Poor perfusion reduces oxygen delivery and leukocyte/collagen function; infection maintains inflammation; tension compromises edge perfusion; dead space separates tissue planes and supports fluid accumulation. Host factors then modify the same biological processes.
NICE surgical-site-infection guidance supports structured wound care, aseptic non-touch dressing changes and appropriate treatment when infection is suspected. Wound-management decisions should follow the wound type, contamination, local policy and tissue-viability expertise rather than a single universal dressing rule.
| Local factors | Systemic factors |
|---|---|
| Poor perfusion/hypoxia, infection, radiation injury, excessive tension | Diabetes, smoking, malnutrition or relevant deficiency |
| Dead space, seroma/haematoma, foreign material and biofilm | Corticosteroids/immunosuppression, anaemia and systemic illness |
| Traumatic tissue handling and devitalised tissue | Frailty, malignancy, chemotherapy or radiotherapy |
8. Hypertrophic scar versus keloid
Risk is influenced by anatomical site, skin phenotype, tension and personal history. Management may involve silicone therapy, pressure, intralesional corticosteroid, laser, surgery with adjuvant treatment or specialist scar services; the choice is individualised.
| Feature | Hypertrophic scar | Keloid |
|---|---|---|
| Boundary | Remains within the original wound | Extends beyond the original wound |
| Timing | Often appears within weeks | May appear later |
| Natural history | May regress with time | More persistent; recurrence after excision alone is common |
| Management | Individualised scar care | Often needs multimodal specialist treatment rather than excision alone |
Active recall
Close the notes and answer these
Try each question from memory before revealing the answer. These public prompts are a small preview of the integrated retrieval system inside SurgAtlas.
01Name the four overlapping phases of wound healing.
Haemostasis, inflammation, proliferation and remodelling.
02Which cell coordinates much of the transition from inflammation to repair?
The macrophage.
03What are the five major processes in the proliferative phase?
Re-epithelialisation, granulation tissue formation, angiogenesis, fibroplasia and wound contraction.
04How does collagen change during remodelling?
Type III collagen is progressively replaced by a higher proportion of type I collagen, with fibre reorientation and increasing cross-linking.
05What is the simplest anatomical distinction between hypertrophic and keloid scars?
Hypertrophic scars stay within the original wound; keloids extend beyond it.
Sources & editorial basis
References & editorial basis
- SurgAtlas production source. Surgical Pathology — Wound Healing & Scarring, including integrated retrieval questions.
- NICE NG125. Surgical site infections: prevention and treatment. Source ↗
This lesson is derived from the corresponding SurgAtlas production teaching material. Where the source makes current management or guideline claims, the public lesson uses the cited contemporary guidance. It is written for education and examination preparation, not as patient-specific clinical advice.
Editorial details
Medical Doctor (MD) · MRCS Part A · Physician · Surgical Educator
SurgAtlas is an educational resource. For patient care, verify current national guidance, local antimicrobial and transfusion policies, specialty pathways and individual patient factors.
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