There are two main types of tissue repair - regeneration and scar formation. Scar formation is a sequential process involving angiogenesis, fibroblast activation and migration, deposition of connective tissue, and remodeling of the scar over time. Factors like infection, steroids, poor perfusion, and foreign bodies can influence the quality of tissue repair. There are also two types of wound healing - healing by first intention which involves minimal scarring, and healing by second intention which involves more extensive tissue loss and granulation tissue formation leading to a larger scar.

1. SCAR FORMATION AND
TISSUE REPAIR

2. SCAR FORMATION
• TISSUES CAN BE REPAIRED BY REGENERATION WITH COMPLETE
RESTORATION OF FORM AND FUNCTION, OR BY REPLACEMENT WITH
CONNECTIVE TISSUE OR SCAR FORMATION
• IT’S A SEQUENTIAL PROCESS INVOLVING THE FOLLOWING STEPS
• ANGIOGENESIS- NEW BLOOD VESSEL FORMATION
• ACTIVATION OF FIBROBLASTS WITH MIGRATION AND PROLIFERATION OF
FIBROBLASTS INTO THE SITEOF INJURY
• DEPOSITION OF CONNECTIVE TISSUE
• REMODELING OF CONNECTIVE TISSUE- THE SCAR CONTINUES TO BE
MODIFIED AND REMODELED

3. FACTORS INFLUENCING TISSUE REPAIR
• THE QUALITY AND ADEQUACY OF TISSUE REPAIR MAY BE AFFECTED
BY THE FOLLOWING FACTORS
• INFECTION: MOST SIGNIFICANT CAUSE OF DELAYED HEALING, IT
PROLONGS INFLAMMATION AND INCREASES THE LOCAL TISSUE
DAMAGE
• STEROIDS: THEY HAVE ANTI-INFLAMMATORY EFFECTS AND DSLOW
THE REPAIR PROCESS
• MECHANICAL EFFECTS; SUCH AS TORSION OR LOCAL PRESSURE
WHICH MAY LEAD TO THE WOUND BEING PULLED APART OR
DEHISCING

4. FACTORS INFLUENCING TISSUE REPAIR
• POOR PERFUSION: IMPAIRMENT IN CIRCULATION DELAYS THE HEALING
PROCESS. CAN BE DUE TO ARTERIAL ISCHEMIA OR IMPAIRED VENOUS
DRAINAGE
• FOREIGN BODY: EG FRAGMNETS OF GLASS, STEEL OR EVEN BONE CAN
PREVENT ADEQUATE HEALING
• TYPE AND EXTENT OF WOUND AND CELL TYPES INVOLVED EG LABILE OR
STABLE CELLS
• LOCATION OF THE INJURY: EG PLEURAL CAVITY MAY HEAL BY FIBROSIS
• ABNORMAL CELL GROWTH AND ECM PRODUCTION: ACCUMULATION OF
EXESSIVE AMOUNT OF COLLAGEN CAUSES KELOIDS

5. SELECTED CLINICAL EXAMPLES OF TISSUE
REPAIR AND FIBROSIS
• HEALING BY FIRST INTENTION
• SIMPLEST EXAMPLE OF WOUND HEALING
• INVOLVES HEALING OF CLEAN, UNINFECTED SURGICAL INCISIONS
APPROXIMATED BY SURGICAL SUTURES
• REFERRED TO AS PRIMARY UNION OR HEALING BY PRIMARY
INTENTION
• INCISION ONLY CAUSES A FOCAL DISRUPTION OF EPITHELIAL
BASEMENT MEMBRANE CONTINUITY AND DEATH OF RELATIVELY FEW
EPITHELIAL AND CONNECTIVE TISSUE CELLS

6. SELECTED CLINICAL EXAMPLES OF TISSUE
REPAIR AND FIBROSIS
• AS A RESULT, EPITHELIAL REGENERATION IS THE PRINCIPAL
MECHANISM OF REPAIR
• A SMALL SCAR IS FORMED, BUT THERE IS MINIMAL WOUND
CONTRACTION
• THE NARROW INCISIONAL SPACE FIRST FILLS WITH FIBRIN CLOTTED
BLOOD WHICH IS THEN RAPIDLY INVADED BY THE GRANULATION
TISSUE AND COVERED BY NEW EPITHELIUM
• THE STEPS IN THE PROCESS ARE WELL DEFINED

7. SELECTED CLINICAL EXAMPLES OF TISSUE
REPAIR AND FIBROSIS
• WITHIN 24 HOURS , NEUTROPHILS ARE SEEN AT THE INCISION
MARGIN, MIGRATING TOWARDS THE FIBRIN CLOT
• BASAL CELLS AT THE CUT EDGE OF THE EPIDERMIS BEGIN TO SHOW
INCREASED MITOTIC ACTIVITY
• WITHIN 24-48 HOURS EPITHELIAL CELLS FROM BOTH EDGES HAVE
BEGUN TO PROLIFERATE ALONG THE DERMIS DEPOSITING BASEMENT
MEMBRANE COMPONENTS AS THEY PROGRESS
• THE CELLS MEET IN THE MIDLINE BENEATH THE SURFACESCAB
RESULTING IN A THIN BUT CONTINUOUS EPITHELIAL LAYER

8. SELECTED CLINICAL EXAMPLES OF TISSUE
REPAIR AND FIBROSIS
• BY DAY 3, NEUTROPHILS HAVE BEEN LARGELY REPLACED BY
MACROPHAGES AND GRANULATION TISSUE PROGRESSIVELY INVADES
THE INCISION SITE
• COLLAGEN FIBRES ARE NOW EVIDENT AT THE INCISION MARGINS BUT
THESE ARE VERTICALLY ORIENTED AND DO NOT BRIDGE THE GAP
MADE BY THE INCISION
• EPITHELIAL PROLIFERATION
• CONTINUES RESULTING IN A THICKENED EPIDERMAL COVERING
LAYER

9. SELECTED CLINICAL EXAMPLES OF TISSUE
REPAIR AND FIBROSIS
• BY DAY 5, NEOVASCULARIZATION RAECHES ITS PEAK AS
GRANULATION TISSUE AS GRANULATION TISSUE FILLS THE
INCISIONAL SPACE
• COLLAGEN FIBRES BECOME MORE ABUNDANT AND BEGIN TO BRIDGE
THE INCISION
• THE EPIDERMIS RECOVERS ITS NORMAL THICKNESS AS
DIFFERENTIATION OF SURFACE CELLS LEADS TO MORE MATURE
EPIDERMAL ARCHITECTURE WITHSURFACE KERATINIZATION

10. SELECTED CLINICAL EXAMPLES OF TISSUE
REPAIR AND FIBROSIS
• DURING THE 2ND WEEK COLLAGEN ACCUMULATION AND FIBROBLAST
PROLIFERATION CONTINUE
• THE LEUKOCYTE INFILTRATION, EDEMA, AND INCREASED VASCULARITY ARE
SUBSTANTIALLY REDUCED
• BLANCHING BEGINS ACCOMPLISHED BY INCREASING COLLAGEN
DEPOSITION WITHIN THE INCISIONAL SCAR AND REGRESSION OF
VASCULAR CHANNELS
• BY THE END OF THE FIRST MONTH THE SCAR CONSISTS OF CELLULAR
CONNECTIVE TISSUE, LARGELY DEVOID OF INFLAMMATORY CELLS COVERED
BY AN ESSENTIALLY NORMAL EPIDERMIS
• HOWEVER APPENDAGES IN THE LINE OF THE INCISION ARE LOST
• THE TENSILE STRENGTH OF THE WOUND INCREASES WITH TIME

11. HEALING BY FIRST INTENTION

12. SELECTED CLINICAL EXAMPLES OF TISSUE
REPAIR AND FIBROSIS
• HEALING BY SECOND INTENTION
• WHEN CELL OR TISSSUE LOSS IS MORE EXTENSIVE SUCH AS IN LARGE
WOUNDS A SITE OF AN ABCESS FROMATION, AN ULCER,ISCHEMIC
NECROSIS IN SOLID ORGANS, THE REPAIR PROCESS REQUIRES A
MORE COMPLEX PROCESS OF REPAIR
• ALSO KNOWN AS HEALING BY SECONDARY UNION
• THE INFLAMMATORY REACTION IS MORE INTENSE AND THERE IS
DEVELOPMENT OF ABUNDANT GRANULATION TISSUE WITH
ACCUMULATION OF ECMAND FORMATION OF A LARGE SCAR
FOLLOWED BY WOUND CONTRACTION

13. SELECTED CLINICAL EXAMPLES OF TISSUE
REPAIR AND FIBROSIS
• IT DIFFERS FROM HEALING BY 1ST INTENTION IN MANY WAYS
• A LARGE CLOT OR SCAB RICH IN FIBRIN AND FIBRONECTIN FORMS AT
THE SURFACE OF THE WOUND
• INFLAMMATION IS MORE INTENSE BECAUSE LARGE TISSUE DEFECTS
HAVE A GREATER VOLUME OF NECROTIC DEBRIS, EXUDATE, AND
FIBRIN THAT MUST BE REMOVED
• CONSEQUENTLY, LARGE DEFECTS HAVE A GREATER POTENTIAL FOR
SECONDARY INFLAMMATORY INJURY

14. SELECTED CLINICAL EXAMPLES OF TISSUE
REPAIR AND FIBROSIS
• LARGE DEFECTS REQUIRE A GREATER VOLUME OF GRANULATION
TISSUE TO FILL IN THE GAPS AND PROVIDE THE UNDERLYING FRAME
WORKFOR THE REGROWTH OF TISSUE GENERALLY RESULTING IN
GREATER SCAR TISSUE MASS
• SECONDARY HEALING INVOLVES WOUD CONTRACTION
• WITHIN 6 WEEKS FOR EXAMPLE A LARGE SKIN DEFECT MAYBE
REDUCED TO 5-10% OF ITS ORIGINAL SIZE DUE TO CONTRACTION

15. HEALING BY SECOND INTENTION

16. HEALING BY FIRST AND SECOND INTENTION

17. SELECTED CLINICAL EXAMPLES OF TISSUE
REPAIR AND FIBROSIS
• WOUND STRENGTH
• CAREFULLY SUTURED WOUNDS HAVE APPROXIMATELY 70% OF THE
STRENGTH OF NORMAL SKIN, LARGELY BECAUSE OF THE PLACEMENT OF
SUTURES
• WHEN SUTURES ARE REMOVED USAULLY AFTER 1 WEEK, WOUND
STRENGTH IS APPROXIMATELY 10% OF THAT OF UNWOUNDED SKIN, BUT
INCREASES RAPIDLY OVER THE NEXT 4 WEEKS
• WOUND STRENGTRH REACHES APPROXIMATELY 70-80% OF NORMAL BY 3
MONTHS AND USUALLY DOES NOT IMPROVE SUBSTANTIALLY BEYOND THIS
POINT

18. FIBROSIS IN PARENCHYMAL CELLS
• DEPOSITION OF COLLAGEN IS PART OF NORMAL WOUND HEALING
• THE TERM FIBROSIS IS USED TO DENOTE THE EXCESSIVE DEPOSITION
• OF COLLAGEN AND OTHER ECM COMPONENTS IN A TISSUE
• SCAR AND FIBROSIS ARE SYNONYMOUS AND ARE USED
INTERCHANGEBLY
• FIBROSIS IS OFTEN RESONSIBLE FOR ORGAN DYSFUNCTION AND
EVEN ORGAN FAILURE EG LUNG FIBROSIS CAUSING RESPIRATORY
FAILURE

19. FIBROSIS

20. FIBROSIS