Phases of Tissue Healing PDF

Phases of tissue healing PT4050 / PT7001 Paul Starrs [email protected] CONTENT S Review the phases of soft tissue healing Content from today is important! Knowledge gained from today will be useful not only for this module but for...

Phases of tissue healing PT4050 / PT7001 Paul Starrs [email protected] CONTENT S Review the phases of soft tissue healing Content from today is important! Knowledge gained from today will be useful not only for this module but for many other elements of the course (and your career!) beyond this point CONTENT S Be able to define what is meant by the term ‘inflammation’, its signs and mediators Differentiate between pathophysiology, features and fate of acute and chronic inflammation Describe the general features of tissue healing such as regeneration and repair and the associated processes Describe the features of healing in soft tissues  INITIATION OF TISSUE HEALING Acute inflammation can be as a result of: Acute trauma Mechanical irritation Thermal insult Chemical insult  PRIMARY AND SECONDARY INJURY Primary injury is the amount of tissue damage caused by the acute trauma – This can be increased by a continuation in aggravating activity but cannot be reduced Secondary injury occurs from hypoxic cell death caused by the subsequent management – Can be decreased Tissue healing refers to the body's replacement of destroyed tissue by living tissue (Walter and BLEEDIN G Sometimes referred to as hemostasis Relatively short lived – 4-6 hours Duration of bleeding will vary depending on structure involved – the more vascular the tissue, the longer it will bleed but the quicker it will repair BLEEDIN G Disruption of blood vessels Immediate, but brief, vasoconstriction of local vessels to limit blood flow to area and prevent excess bleeding, followed by vasodilation once clot formed by fibrin and fibronectin INFLAMMATIO N NORMAL reaction of the body to tissue damage Essential component, rather than inappropriate reaction, as: Removal of damaged and dead tissues Prepares body to repair Onset and resolution are swifter in more vascular tissues and slower in the relatively poorly vascularised tissues “-itis” is a suffix which usually indicates a condition with inflammation presence  CARDINAL SIGNS OF INFLAMMATION LOSS OF HEAT REDNESS SWELLING PAIN FUNCTION Caused Stimulati Increase by Caused on of d accumul by pain chemical ation of Resultant dilation detecting activity & blood, of of blood nerve increase lymphati increase vessels & endings. d blood c fluid d pain & increase Increase flow to and swelling d blood in skin damaged flow chemical surface tissue irritants cells INFLAMMATIO N Rapid onset after acute injury Maximal reaction 1-3 days following Numerous chemical mediators involved e.g. IGF, prostaglandins, growth factors, etc. Two cascading components which occur in parallel and are significantly interlinked: Vascular events Cellular events  VASCULAR EVENTS 1. VASODILATION 2. An increase in VASOPERMEABILITY  VASCULAR EVENTS Vasodilation follows brief period of vasoconstriction (mediated by histamine and prostaglandins) More volume present and therefore more platelets and white blood cells migrate Previous dormant capillaries are opened An increase in vasopermeability is mediated by release of chemicals such as histamine and serotonin Leakier cell membranes, increase volume, flow and pressure cause smaller solutes to pass into tissue spaces Increase presence of plasma proteins causes an attraction, and the retention, of fluid which  CELLULAR EVENTS Emigration of phagocytes e.g. neurtrophils (white blood cells that fight infection and bacteria) help to protect from infection Remove tissue debris e.g. dead/dying cells, fibrin mesh/clot, all need to be removed As a bonus, one of the chemicals released as an end product of phagocytosis is lactic acid which is one of the stimulants of proliferation  CHRONIC INFLAMMATION May follow on from a prolonged acute inflammatory reaction or in fact develop slowly with no initial acute phase (insidious onset) Insidious onset of inflammation may be caused by local irritants, poor circulation, some micro-organisms or immune disturbances Usually more productive as attempting to produce fibrous material to aid PROLIFERATIO “TO INCREASE RAPIDLY IN N NUMBER” Also referred to as the regeneration phase Restoration of repair tissue Extends from 48 hours to 3-6 weeks PROLIFERATIO N There are two processes involved in the temporary repair procedure: 1. Formation of fibroblasts (fibroplasia) 2. Angiogenesis  FIBROBLAST FORMATION A fibroblast is a cell that manufactures and maintains connective tissue. In the human body, this connective tissue is called COLLAGEN During proliferation, fibroblasts will migrate to the injured area (as a result of chemical mediators (Macrophage Derived Growth Factors) released by the macrophages during inflammation) and start to produce new collagen to replace the dead/dying tissue Initially, type III collagen will be produced which has a granular ANGIOGENESI LATIN FOR BLOOD VESSEL “TO CREATE” S Capillaries bud in area to provide cells with blood which provide the oxygen required for metabolism, as well as removal of metabolic and repair waste products REMODELLIN G Refinement of the collagen and its extracellular matrix The initial deposition of collagen produces relatively weak fibrils with random orientation With maturity, the collagen increases in tensile strength and is oriented in line with local stresses (tissue loading via exercise is key!) Overall, type III collagen matures, or is reabsorbed, into type I collagen Can last up to 12 months post injury INJURED AND HEALTHY TENDON TISSUE COLLAGEN STRENGTH PROLIFERATION AND REMODELLING  FACTORS THAT AFFECT HEALING Age Smoking Long term steroid use NSAID's Temperature (lower rate when colder) Poor blood supply / ischaemia Excessive movement or mechanical stress  INJURY MANAGEMENT AND HEALING Effects of treatment and exercise prescription appear to be achieved by 'stimulating' rather than 'changing' the events during healing Inappropriate therapy at any stage is capable of inhibiting these events and therefore results in poorer tissue repair Treatment is not guaranteed to be beneficial – you have to be mindful of the cellular and tissue events and be selective of the most appropriate and evidence based intervention at each stage SUMMARY Four phases of healing: 1. Bleeding 2. Inflammation 3. Proliferation 4. Remodelling Inappropriate therapy at any stage is capable of inhibiting these events and therefore results in poorer tissue repair  ANY QUESTIONS?