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Healing of tissues
1. Healing of tissues occurs through regeneration or repair depending on the capacity of cells to divide. Regeneration involves replacement with the same type of cells while repair involves replacement with fibrous tissue. 2. Granulation tissue formation and wound contraction are the two main processes involved in repair. Granulation tissue forms through angiogenesis and fibrogenesis. 3. Fracture healing occurs through either primary or secondary union depending on the stability of the fracture. Secondary union involves procallus formation, osseous callus formation and remodeling of the bone.
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Healing of tissues
- 1. HEALING OF TISSUES SYAMAM P THRISSUR GOVERNMENT DENTAL COLLEGE
- 4. REGENERATION • Some parenchymalcell are short lived while others have longer life span • Depending on capacity to divide cells are divided to 1.labile cells: continue to divide throughout life eg: epithelial cells of epidermis, GIT ,respiratory tract ,cervix vagina endometrium hematopoietic cells of bone marrow cells of lymph nodes spleen 2.stable cells : Lose their ability to divide after adolescence but retain the ability to divide in response to a stimuli through out their life eg: vascular endothelium,fibroblasts, mesenchymal cells like smooth muscle cells bone cartilage cells parenchymal cells of organs like liver spleen kidney adrenal thyroid 3.parenchymal cells: They lose their ability to proliferate around time of birth eg: skeletal muscle nervous tissue and cardiac muscle
- 5. REPAIR • Replacement ofinjured tissue by fibrous tissue • Includes 2 processes • 1.. Granulation tissue formation • 2..Contraction of wounds • GRANULATION TISSUE FORMATION • Granular : corresponds to new blood vessels with thin covering of fibroblast and young collagen , which seems to be slightly lifted on the surface • Pink in colour
- 6. PHASES OF GRANULATIONTISSUE FORMATION • 1.Phase of inflammation • 2.Phase of clearance • 3.Phase of ingrowth of granulation tissue • a.Angiogenisis • b. Fibrogenesis
- 7. ANGIOGENESIS (NEOVASCULARISATION) • Proliferationofendothelial cells from the margins of severed blood vessels. • Initially, the proliferated endothelial cells are solid buds • Within a few hours develop a lumen and start carrying blood. • The newly formed blood vessels are more leaky, accounting for the oedematous appearance of new granulation tissue. • Soon, these blood vessels differentiate into musculararterioles, thin-walled venules and true capillaries. • The process of angiogenesis is stimulated with proteolytic destruction of basement membrane. • Angiogenesis takes place under the influence of following factors: • a) Vascular endothelial growth factor (VEGF) bymesenchymal cells • b) Platelet-derived growth factor (PDGF) • c)Transforminggrowth factor-ß (TGF-B) • d)Basic fibroblast growth factor(bFGF) • e) Surface integrins are all associated with cellularproliferation.
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- 9. FIBROGENISIS • The newlyformed blood vessels are present in an amorphous ground substance or matrix. • The new fibroblasts have features intermediate between those of fibroblasts and smoothmuscle cells (myofibroblasts). • Collagenfibrils begin to appear by about 6th day. • The myofibroblasts have surface receptors for fibronectin molecules which form bridges between collagen fibrils. • As maturation proceeds,more and more collagen is formed while the number of active fibroblasts and new blood vessels decreases. • This results information of inactive looking Scar • This process is known as cicatrisation.
- 10. PRIMARY UNION • Thisis defined as healing of a wound wlhich has the followingcharacteristics: • i) clean and uninfected; • ii) surgically incised; • ii) without much loss of cells and tissue; • iv) edges of wound are approximated by surgical sutures. • 1.. Initial haemorrhage Immediately after injury, theSpace between the approximated surfaces of incised woundis filled with blood which then clots and seals the woundagainst dehydration and infection • .2. Acute inflammatory response This occurs within24 hours with appearance of polymorphs from the marginsof incision. By 3rd day, polymorphs are replaced bymacrophages. • 3. Epithelial changes Basal cells of epidermis from boththe cut margins start proliferating and migrating towardsincisional space in the form of epithelial spurs. A well-approximated wound is covered by a layer of epithelium in48 hours. The migrated epidermal cells separate theunderlying viable dermis from the overlying necrotic materialand clot, forming Scab which is cast off. The basal cells fromthe margins continue to divide. By 5th day, a multilayered newepidermis is formed which is differentiated into superficialand deeper layers. • 4. Organisation By 3rd day, fibroblasts also invade thewound area. By 5th day, new collagen fibrils start formingwhich dominate till healing is completed. In 4 weeks, theScar tissue with scanty cellular and vascular elements, a fewinflammatory cells and epithelialised surface is formed.
- 12. • 5. Suturetracks • Each suture track is a separate wound and incites the same phenomena as in healing of theprimary wound • When sutures are removed around 7th day, much of epithelialised suture track is avulsed and the remaining epithelial tissue in the track is absorbed. • However, sometimes the suture track gets infected (stitch abscess), or the epithelial cells may persist in the track(implantation or epidermal cysts). • Thus, the scar formed in a sutured wound is neat due to close apposition of the margins of wound; the use of adhesive tapes or metal clips avoids removal of stitches and its complications.
- 13. HEALING BY SECONDINTENTION (SECONDARY UNION) • This is defined as healing of a wound having the followingcharacteristics • :open with a large tissue defect, at times infected;n • having extensive loss of cells and tissues; • the wound is not approximated by surgical sutures but isleft open. • Healing takes place from the base upwardand also from the margins inwards. Healing by second intention is slow and results in a large, at times ugly, scar as compared to rapid healing and neat scar of primarv union)
- 14. • 1. Initialhaemorrhage • 2.Inflammatory response • . Epithelial changes :As in primary healing, the epidermal cells from both the margins ol wound proliferateand migrate into the wound in the form of epithelial spurs till they meet in the middle and re-epithelialise the gapcompletely • . However, the proliferating epithelial cells do not cover the surface fully until granulation tissue from base has started filling the wound space. I • n this way, pre-existing viableconnective tissue is separated from necrotic material and clot on the surface, forming scab which is cast off • In time, there generated epidermis becomes stratified and keratinised.
- 15. • 4. Granulationtissue • Main bulk of secondary healing is by granulations. • The newly-formed granulation tissue is deep red,granular and very fragile. • With time, the scar on maturation becomes pale and white due to increase in collagen and decrease in vascularity. • Specialised structures of the skin like hair follicles and sweat glands are not replaced unless theirviable residues remain which may regenerate • .5. Wound contraction Contraction of wound is an important feature of secondary healing, not seen in primaryhealing. • Due to the action of myofibroblasts present in granulation tissue, the wound contracts to one-third to one-fourth of its original size.
- 16. • 6.Presence ofinfection Bacterial contamination lead to necrosis suppuration thrombosis • Surgical removal of dead and necrosis tissue debridement help in preventing this • COMPLICATIONS OF WOUND HEALING • 1. Infection The wound may get infected due to entry bacteria which delays the healing. • 2. Implantation (epidermal) cyst Formation of implantaticepidermoid cyst may occur due to persistence of epithelial cells in the wound after healing • .3. Pigmentation Healed wounds may at times have rust-like colour due to staining with haemosiderin.
- 17. • Some colouredparticulate material left in the wound may persist and impart colour to the healed wound • 4. Deficient scar formation This may occur due to inadequate formation of granulation tissue. • 5. Incisional hernia A weak scar, especially after a laparotomy, may be either the site of bursting open of a wound early (wound dehiscence), or later an incisional hernia may occur at this site • .6. Hypertrophied scars and keloid formation At times,the scar formed is excessive, ugly and painful. Excessive formation of collagen in healing may result in keloid(claw-like) formation, seen more commonly in blacks .Hypertrophied scars differ from keloid in that they areconfined to the borders of the initial wound while keloid have tumour-like projection of connective tissue. • 7. Excessive contraction An exaggeration of wound contraction may result in formation of contractures or cicatrisation e.g. Dupuytren's (palmar) contracture, plantar contracture and Peyronies disease • Neoplasia
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- 19. BASED ON STABILITY PRIMARYUNION OF FRACTURES • Small amount of strain below 2% then it heals by primary union • They can be approximated by compression clamps and metal plates • No procallus formation only osseous callus formation and then remodelling • More extensive bone necrosis • Slow healing SECONDARY UNION OF FRACTURES • Strain from 2% to 10 % • Part is immobilized by plaster cast • It’s a continuous process • Fast healing • 1.Procallus formation • 2. Osseous callus formation • 3. Remodelling
- 21. PROCALLUS FORMATION • Hematoma• Local inflammatory response • From the leaky blood vessels Exudation of fibrin polymorph and macrophages • Macrophages clears all the debris • Fragments of enclosed bone removed by osteoclasts and macrophages
- 22. • INGROWTH OFGRANULATION TISSUE • Begins with neovascularisation • Then proliferation of mesenchymal cells • Mesenchymal cells are multi potent stem cells that can differentiate and form chondrocytes osteoblasts • They are from periosteum and endosteum • Thus soft tissue callus is formed they unite the fractured ends
- 23. • 4 Calluscomposed of woven boneand cartilage • Startswithin the first few days • The cells of inner layer of the periosteum have osteogenic potential and lay down collagenas well as osteoid matrix in the granulation tissue • .The osteoid undergoes calcification and is called woven bone callus. • A much wider zone over the cortex on either side of fractured ends is covered by the woven bone callus and united to bridge the gap between the ends, giving spindle-shapedor fusiform appearance to the union. • In poorly immobilised fractures (e.g. fracture ribs), the.subperiosteal osteoblasts may form cartilage at the fracture site. At times, callus is composed of woven bone as well as cartilage, temporarily immobilising the bone ends.
- 24. • The procallushas external intermediate and internal procallus
- 25. OSSEOUS CALLUS FORMATION •Procallus act as scaffolding on which osseous callus with lamellar bone is formed • Osteoclasts will clear away woven bone • Calcified cartilage disintegrates • In that place new blood vessels and osteoblasts invade • They lay down osteoid that is calcified and lamellar bone is formed
- 26. REMODELLING • During theformation of lamellar bone,Osteoblastic laying and osteoclastic removal are taking place remodelling the united bone ends, which after sometime, is indistinguishable from the normal bone • External callus cleared away • Intermediate callus become cortex • Internal callus become bone marrow