1. Concepts of Healing

2.  https://www.youtube.com/watch?v=suCK m97yvyk

3. Healing Phases- Inflammation  Injury occurs and body starts defense  Goal of rehab clinicians is to allow inflammation to happen, but minimize it

4. Inflammation-Vasoconstriction and vasodilatation  Vasoconstriction limits oxygen which triggers the inflammation process by causing hypoxia  Vasodilatation releases blood and blood products to injured site

5. Inflammation- Cellular Response  Chemicals are released and other cells attracted  Platelets  release phospholipids (stimulate clotting)  Bind to collagen  Release fibronectin, growth factors, fibrinogen

6.  Fibronectin binds fibrin and collagen to form web to stop bleeding  Eventually replaced by Type III collagen  Damaged lymph vessels also plugged  Since they are plugged, can’t evacuate extra fluid  Once the area is stable, chemical released to promote absorption of fibrin plug

8.  To remove debris, neutrophils (WBC) come in 5-6 hours after injury  Neutrophils replaced by phagocytes, monocytes, and macrophages to remove debris and dead tissue  24-48 hours post injury  Exudate formed from fluid escaping vessels, dead tissue  Debridement needed for healing to continue

9. Inflammation- Chemical Reactions  Some cells produce chemicals, and some chemicals stimulate the arrival or production of specific cells.  Chemotaxis- the process of attraction or stimulation  Vascular permeability caused by histamine that is released by mast cells  Histamine is a chemotactic factor for WBC  Kinins released by plasma  Prostaglandin forms (continues vascular permeability, attracting leukocytes). These permit advancement to Proliferation Stage

10. Proliferation  Fibroblasts- responsible for new capillaries and extracellular matrix  Matrix protects new blood vessels  Collagen produced is Type III- weak, thin, haphazard  Tensile strength is directly related to amount, type, & arrangement of collagen

11. Remodeling Phase  Wound tissue converts to scar tissue  Type I collagen synthesized, Type III destroyed  More resistant to destruction  As fluid reduces, can create more cross links

12. Specific Tissue  Ligaments  Injured ligament stumps surrounded by fluid

13. Tendons  Have support from structures that aid in healing  Periosteum  Synovial sheath  Collagen synthesis weeks 1-4  Week 2 cells begin to align along lines of stress  Revasularization in first 3 weeks  Immobile until day 21  Week 3 synovial sheath reconstituted

14. Muscles  Satellite cells  Unique to muscles  Fuse with adjacent myofibribers to repair  Occurs daily  Larger muscles resort to scar tissue

15. Articular Cartilage  Made of Type II collagen  Cartilage regenerates slower than scar tissue  Healing depends on  Depth of defect  Maturity of cartilage  Location of defect  Surgical repair options  Clean the joint  Lavage or debridment  Repair the joint  Arthroplasty, drilling, microfracture  Restore the joint  Plugs and transplantation

16. Bone  Callus takes 3-4 weeks to form  Eventually becomes bone  Immobilizes fragment ends, allows stress to be applied without harming fracture site

17. Specific Tissue TissueInflamProlifRemodFinal Ligament 0-72 hrs 1-6wk 6wk- 12mo 40-50wk Tendon0-1wk10d-42d 2mo- 112d 40-50wk Muscle0-1wk7-18d6wk-6mo6mo Articular cartilage 0-5d2wk-1mo2mo6mo Bone0-4d1-6wk3-4mo12wk

18. Factors the Affect Healing  Modalities  Drugs  Surgical repair- quality of technique, follow up, infection  Age  Disease  Wound size  Infection  Nutrition  Muscle spasm  Swelling

19. Healing & Rehab Timeline Inflammation Modalities for reduction of pain, muscle spasm, edema. No exercises to disrupt fibrin plug. Exercise non-involved body parts, cardio Proliferation Modalities, non-involved and cardio ROM to influence collagen arrangement- mild PROM, AAROM, some AROM Mild isometrics Remodeling Move from full motion to resistive exercises Progress to balance and agility Functional and sport-specific toward end Aggressiveness inc as tissue strength improves