1. Ch. 2
Tissue Healing

2. Introduction
Tissue healing occurs and is influenced by several factors
There are three phases:
Inflammatory response
Repair/regeneration
remodeling

3. Inflammatory Response
Cells remove debris
Cells create groundwork for repair and regeneration phase

4. Repair/Regeneration Phase
Cells restore the vascular and structural integrity of injured structures

5. Remodeling Phase Healed tissue adapts to functional loading
Gets stronger based on the stress that is applied to it
The three phases overlap one another
Disruption of any one phase can cause an unsatisfactory outcome

6. Types of Tissue
Epithelial tissue
Connective
Muscle
nervous

7. Epithelial Tissue Composed of layers of cells Protect organs
Secretions (glands)
Absorption ( lining of the stomach )

8. Connective Tissue Most abundant and variable tissue in the body
Attaching organs
Support/structure
Movement
Physical protection
Immune response, energy & mineral storage
Heat generation and transportation (blood, etc.)

9. Connective Tissue Subtypes: Fluid connective tissue=blood and lymph
Fibroconnective tissue=fat, tendons and ligaments
Supportive connective tissue=cartilage and bone

10. Nervous Tissue Located in brain and spinal cord and nerves
Electrically exciteable
Used to transmit and respond to various impulses and forms of information

11. Muscle Tissue Skeletal- striated or voluntary Cardiac – heart muscle
Smooth- linings of organs and blood vessels

13. Common Injuries

14. Puncture and Laceration

15. Incision

16. Acute vs. Chronic Acute – single forcefull event (ACL tear)
Chronic – occur over a period of time (Tennis elbow)

17. Acute Injuries Contusions – bruises
Strains – muscle or tendon injuries
Sprains – ligamentous injuries

18. Contusions Caused by compressive forces
or direct impacts and are graded by degrees of trauma
1st degree-minimal swelling, no limits
2nd – pain, bleeding, moderate functional limits
3rd-hematoma formation,sever limitations

19. Sprains and Strains

20. Fracture Classifications
Greenstick
Transverse
Oblique
Spiral
Comminuted
Avulsion
Impacted
Depressed
Epiphyseal (Salter-Harris classification)

21. Peripheral Nerve Injuries
Neuropraxia-least severe, transient and reversible loss of nerve function
Axontomesis- partial disruption, may cause atrophy or weakness for 2 – 52 weeks
Neurotomesis – complete severance of a nerve resulting in permanent loss of function

22. Chronic Injuries Blisters – continuous friction
Repetitive overload – tendinosis, tenosynovitis
Chronic irritation –could cause neuralgia or neuroma

23. Soft Tissue Healing Phase 1: Inflammatory Response
Phase 2: Repair/Regeneration
Phase 3: Remodeling/Maturation

24. Phase 1 Signs and symptoms: Redness Heat Pain Swelling
Loss of function

25. Phase 1 con’t Lasts 7-10 days
Initial damage is called “the primary injury”
Caused by a release of proteins at the injury site
Mast cells produce chemicals (histamines) which promote vasodilation
This causes the redness and heat
Vessels become more permeable which contributes to the swelling

26. Phase 1
Mast cells also release chemicals that attract neutrophils (immune cells) to come to the injury
Neutrophils clear debris and regulate the early inflammatory process
Injured area becomes ischemic and acidic which may cause secondary damage to otherwise healthy areas around the injury

27. Phase 1
Neutrophils die and are ingested by macrophages at the injury site
When this happens the macrophages begin to produce proteins that promote tissue repair
Early scar tissue forms
Early rehab should focus on pain management, decreasing swelling, promote tissue healing

28. Phase 1 Immobilization or protection should be done RICE
NSAIDS for decreased inflammatory symptoms
Short term analgesic

29. Phase 2: Repair/Regeneration
Repair- articular cartilage, meniscus, spinal cord (new tissue is not identical)
Regeneration- bone, muscle, peripheral nerve, blood vessels (heal with identical tissue)
Patients are still swollen and pain with motion
Blends with the inflammatory phase and remodeling phase
Day 7 to 21

30. Phase 2 Fibrin clots form Fibroblasts proliferate near the injury
Capillary proliferation occurs (more oxygen needed)
Fibroblasts produce fibronectin, collagens, glycoproteins
Fibronectin begins dormant followed by type III collagen then to stronger type I

31. Phase 2 Initially patient has structural deficiency
Treatment – early controlled mobilization
This aligns collagen with areas of physical stress making it stronger
Prevents atrophy

32. Phase 3: Remodeling/Maturation
Lasts up to 24 months
May have persistent swelling and pain with motion
Fibroblast activity decreases throughout this phase
Capillary density decreases
Cellular matrix becomes more refined

33. Phase 3 More type I and type III collagen fibers are produced
Tensile strength improves
Rehab can increase the physical demands until patients return to their activities of daily living

34. Fracture Healing Four phases: Inflammation Soft callus formation
Hard callus formation
Bone remodeling

35. Phase 1: Acute Lasts up to a week
Hematoma formation, inflammation, angiogenesis (new blood vessel formation), soft callus formation
Dominated by immune cells
Phagocytic cells remove debris
Platelets form clots

36. Phase 2: Repair/Regeneration
Lasts 8 to 12 weeks
Remodeling of scar tissue through cartilage formation, calcification and bone formation
Mesenchymal cells become cartilage cells
Proliferate the soft callus
Replace the scar tissue with cartilage
Chondrycytes hypertrophy and release chemicals to promote bone formation

37. Phase 2 Osteoblasts produce new bone
Revascularization of the region occurs
Soft tissue is replaced by bone
Casting is used to allow time for a proper callus to develop

38. Phase 3: Remodeling
Starts during Phase 2 and continues for several years
Starts 21 days post fracture
Woven bone replaced by cortical or trabecular bone
New bone is remodeled by osteoclasts and osteoblasts based on mechanical loading

39. Fracture Management Treatment varies by : type of fixation
No reduction
Closed reduction
Open reduction
Open reduction internal fixation (ORIF)
Location of fx
Involved bone
Mechanical loads
Surrounding soft tissue

40. Fracture Management ORIF Surgical fixation
Uses metal implants to stabilize fx’s
May allow rehab to begin within first week after surgery ( edema control, wound management, early motion)
More aggressive rehab can begin in 6-8 weeks

41. Fracture Management Non-surgical fixation ROM delayed for 3 weeks
Until callus has enough tensile strength to tolerate movement
At 6-8 weeks patient may begin strengthening exercises and increase mechanical loads
Upper extremity fx’s may begin ROM exercises sooner because of smaller loads and fear of atrophy

42. Delayed/Non Union Fx’s
Causes
Nutritional deficiencies
Diabetes, anemia
Smoking
Pharmacological drug use
Pre-injury vascular status
Muscle around fracture
Inadequate immobilization
Infection
High energy fractures
Gap distance
Nerve injury

44. Delayed / Non Union Fx’s
Susceptible areas
Tibia
Ulna
Femoral neck
Scaphoid (most common)

45. Peripheral Nervous Healing
More proximal injuries result in greater losses
Within 3 -5 days, axons distal to the injury undergo a degenerative process called Wallerian degeneration
This is promote by immune cells, Schwann cells(the cell that normally myelinate axons) and the distal axon

46. Nerve Healing
Produce proteins that produce and inflammatory response and pain
Schwann cells divide to create an optimal environment for regeneration
Surgical repairs can be helpful but are not guaranteed
Only one proximal branch will form a new axon the others will degenerate

47. Muscle Healing Tissue trauma Hematoma formation
Inflammatory cell reaction
Phagocytosis
Capillary regrowth
Scar formation
remodeling

48. Muscle Healing Must balance regeneration with scar formation
Scar tissue is weak and only serves as a “scaffold” for the healing process
Site is still weak
No active motion immediately after injury
Could result in re-rupture
However, prolonged immobilization could result in atrophy

49. Muscle Healing
What do you do?

50. Muscle Healing
Early mobilization and motion may be started within the first 24 hours
It must be pain free to avoid overloading
Pain is your guide

51. Tendon Healing Ruptured tendons often require surgery
Once repaired the tendon ends can go through their normal healing stages

52. Tendon Healing Hematoma formation Platelet aggregation
Recruitment of inflammatory cells
Phagocytosis
Angiogenesis
Fibroblast proliferation
remodeling

53. Tendon Healing Tensile strength increases at 4 weeks
Continues to improve up to 1 year
Strength of tendon never returns to pre-injury level

54. Factors Affecting Healing
Healing process is variable
Factors:
Extensive trauma
Blood supply
Infection
Diabetes
Age
nutrition

55. Critical Thinking
In a rehab setting, patients want to return ASAP. As a result, some patients do extra exercises, stretch to a point of pain, or try aggressive exercises (e.g. running) too early. What are the potential hazards to this approach? How would you explain your concerns to the patient or athlete?

56. Critical Thinking
Two patients that are 10 weeks post –fractures are exercising next to each other. One of the patients had a distal radius fracture and the other had a scaphoid fracture. Both were treated conservatively with immobilization. The patient with the scaphoid fracture notices that she is still not able to do a lot of the exercises her counterpart is able to perform. She then asks why she is not progressing at the same rate as the other patient. How would you explain the differences in their recovery?