> ## Content Index > Fetch the complete content index at: https://www.theplasticsfella.com/llms.txt > Use this file to discover other available public pages before exploring further. # Wound Healing - URL: https://www.theplasticsfella.com/wound-healing/ - Published: 2022-04-01T17:56:00.000Z - Updated: 2025-12-15T19:41:29.000Z - Description: Wound Healing is most commonly by primary and secondary intention. It involves hemostasis, inflammation, proliferation and remodelling. - Author: PlasticsFella - Tags: Core Principles 👇 **In this Article** [5 Key Points on Wound Healing](https://www.theplasticsfella.com/wound-healing/#5-key-points-on-wound-healing) [Types of Wound Healing](https://www.theplasticsfella.com/wound-healing/#types-of-wound-healing) [Phases of Wound Healing](https://www.theplasticsfella.com/wound-healing/#phases-of-wound-healing) [Re-epithelialisation ](https://www.theplasticsfella.com/wound-healing/#re-epithelialisation-in-wound-healing) [Contraction ](https://www.theplasticsfella.com/wound-healing/#contraction-in-wound-healing) [Factors affecting wound healing](https://www.theplasticsfella.com/wound-healing/#wound-healing-factors) [Flashcards](https://www.theplasticsfella.com/wound-healing/#flashcards) --- ## 5 Key Points on Wound Healing #### 1\. Types of Wound Healing Wound Healing can be via primary, secondary or tertiary intention #### 2\. Phases of Wound Healing Phases of wound healing are hemostasis, inflammation, proliferation and remodelling. #### 3\. Important cells in wound healing Macrophages, neutrophils and fibroblasts play integral roles in activating pathways, reducing bacterial burden, and promoting collagen formation, respectively. #### 4\. Re-epithelialisation vs Contraction Re-epithelialisation occurs in wounds with an intact epidermal basement membrane via mobilisation, migration, mitosis and differentiation. Contraction occurs in wounds after 3 days and is caused by myofibroblasts. #### 5\. Factors affecting healing There are genetic conditions, acquired systemic issues and local factors that all influence wound healing. ### --- ## Types of Wound Healing There are 3 ways a wound can heal: 1. **Primary closure:** most common 2. **Secondary intention:** open wound that granulates, contracts, epithelialises 3. **Tertiary Intention:** delayed primary (a wound that is closed at a later date) Here is an in-depth video tutorial. --- ## Phases of Wound Healing There are 4 phases to wound healing: **haemostasis**, **inflammation**, **proliferation** and **remodelling**. These stages are the same for both primary and secondary intention healing. ![A healing wound has 4 phases: haemostasis, inflammation, proliferation and remodelling](https://storage.ghost.io/c/a0/9f/a09fd7b4-d396-4b28-aed3-b87e20483292/content/images/2022/06/Phases-of-Wound-Healing.png) Phases of Wound Healing ### 1\. Haemostasis This occurs acutely and is initiated once a wound has been created. The key aspects of this include: - **Vasoconstriction** from thromboxane & prostaglandins release. - **Activating** platelet-activating factor, von Willebrand, & thromboxane A2\. - **Platelet plug** formation secondary to platelet activation - **Thrombus** formation is secondary to fibrinogen converted to fibrin. This can **weakly** hold the wound together. 💡 At a **cellular** level, **macrophages** release inflammatory **cytokines** and engage in **phagocytosis**, and **neutrophils** infiltrate the wound. ### 2\. Inflammation This occurs within the first 72 hours of the initial activation of the wound healing pathway. The key aspects of this include: - **Cell proliferation** is secondary to the release of platelet-derived growth factors and pro-inflammatory factors (serotonin, bradykinin, histamine). - **Vasodilation** as endothelial cells swells and polymorphonuclear neutrophils travel into the tissue. - **Cellular immunity and antibody production** from T-lymphocytes entering the wound (influence by interleukin-1) and secreting cytokines. 💡 At a **cellular** level, **macrophages** become the dominant cell within 48 hours of the injury until **fibroblast** proliferation. The final cell line is **lymphocytes**. ### 3\. Proliferation This occurs after \~72 hours and is usually complete within 2-4 weeks. The key aspects of this include: - **Matrix formation** fromfibroblasts& glycosaminoglycan production. - **Collagen & elastin production** is secondary to fibroblasts (mainly type III). This can hold the wound together quite strongly. - **Wound contraction** as fibroblasts differentiates into myofibroblasts. - **Angiogenesis** secondary to endothelial stem cell migration. This is assisted by macrophages stimulating nearby vascular endothelium of adjacent capillaries. 💡 **Glycosaminoglycans** production includes hyaluronic acid, chondroitin-4 sulfate, dermatan sulfate and heparin sulfate. ### 4\. Remodelling This occurs after 2-4 weeks from injury and can last >1 year. This phase of wound healing is responsible for the tensile strength of a wound. The **key** aspects of this include: - **Collagen Haemostasis:** no increase in collagen production - **Collagen replacement**: type III collagen is replaced by type I (stronger). - **Collagen re-organisation:** becomes organised with stronger cross-links. - **Apoptosis** removes the capillary network and creates a pale-looking scar. 💡 **Tensile strength** increases at \~day 5 & is 80% pre-injury at \~60 days. The type of cell involved in wound healing changes over time. The first cells are predominantly neutrophils. After 48 hours, macrophages become dominant during the inflammatory phase. Fibroblasts and myofibroblasts play an important role in proliferation and remodelling. --- ## Re-epithelialisation in Wound Healing This is the process of re-establishing epithelial continuity through 4 phases: **mobilisation**, **migration**, **mitosis**, and **differentiation**. Re-epithelialisation occurs after the basement membrane of the [epidermis](https://www.theplasticsfella.com/anatomy-of-the-skin/) has been breached. It occurs from the edges of the wound and [epidermal appendages](https://www.theplasticsfella.com/anatomy-of-the-skin/). The 4 phases of re-epithelialisation are as follows: 1. **Mobilisation:** epithelial cells lose contact with neighbours (contact inhibition) to become flat and long and form pseudopodia. 2. **Migration:** epithelial cells attempt to overcome contact inhibition by moving centrally. 3. **Mitosis**: epithelial cells proliferate once, desmosomes and hemidesmosomes attach to the basement membrane and form a [stratum germinativum](https://www.theplasticsfella.com/anatomy-of-the-skin/). 4. **Differentiation**: cells differentiate to recreate normal stratified squamous epithelium. 💡 If the **basement membrane** is intact then the epithelial cells are replaced by upward migration of keratinocytes. --- ## Contraction in Wound Healing Contraction occurs in the granulating wound when myofibroblasts contract the wound bed. Contraction is a normal phenomenon in a granulating wound bed due to myofibroblasts. Here are some key points on myofibroblasts - First appear \~72 hours after injury and peak at 2-3 weeks. - Contain contractile microfilaments and distinct cellular adhesions (desmosomes and maculae adherens) - Disappear when contraction is complete 💡 Tip: There is **less** contraction when there is **more** dermis. --- ## Wound Healing Factors Wound healing is influenced by medical conditions, systemic factors and local factors. ### Medical conditions The following medical conditions negatively influence the ability of a wound to heal: 1. **Pseudoxanthoma elasticum:** increased collagen degradation giving a pebble-skin appearance. 2. **Epidermolysis Bullosa:** skin is very delicate 3. **Ehler's Danlos Syndrome:** abnormal collage structure 4. **Cutis Laxa:** mutated elastic fibres presenting in newborns as excessive laxity. 5. **Werner Syndrome:** mutated WRN gene presenting similarly to scleroderma. 6. **Progeria:** mutated LMNA gene creating an appearance of "premature ageing". 💡 Clinical Gem: blistering after minor trauma in patients with epidermolysis bullosa is called Nikolsky Sign. ### Systemic Factors The following systemic factors play an important role in wound healing. 1. **Age**: as you age so too does your ability for cell re-growth and tensile strength. 2. **Smoking:** nicotine induces vasoconstriction, carbon monoxide decreases oxygen-carry capacity, and hydrogen cyanide impairs oxygen transport 3. **Comorbidities:** for example diabetes. 4. **Nutrition:** vitamin A (retinol) and C are required for collagen cross-linking and synthesis, respectively. Vitamin E stabilises the membrane. Low albumin is a predictor of poor wound healing. 5. **Medication:** steroids inhibit epithelialisation & decrease collagen production. ### Local Wound Factors Local wound issues are usually the most common reason for delayed wound healing. It can relate to: 1. **Infection**: reduces oxygen tension, pH, epithelialisation and angiogenesis, whilst increasing collagenase activity and inflammation 2. **Radiation**: occludes small vessels, and damages fibroblasts and nuclei. 3. **Temperature**: warm and moist increase epithelialisation and tensile strength. 4. **Oxygen delivery**: microvascular disease results in reduced tissue perfusion. 💡 In a **chronic wound**, the wound is slow to heal due to excessive **metalloproteases** which promote matrix turnover. --- ## Flashcards ⚡ Evidence-based flashcards are designed for active recall and spaced repetition of the verified information you are currently studying. They are continually updated and are for thePlasticsPro users.