Muscle/tendon/bone healing

Question 1

Muscle Haematoma/Inflammatory Phase

Answer 1

Day 0-4
-Mechanical trauma destroys the integrity of the myofibre plasma membrane and basal lamina, and the cellular contents and chemotactic factors are released into the extracellular space.
-In turn, this induces the infiltration of many types of immune cells (eg mast cells and neutrophils).
-As the degradation of muscle proteins and apoptosis occurs (the necrosis of fibres injured beyond repair), these phagocytes help to clear the damaged myofibres at the injury site (phagocytosis).
-The muscle degeneration is further promoted by swelling and formation of haematoma as a consequence of the activation of acute inflammation.
-The phagocytes also secrete various types of cytokines to recruit more immune cells, such as macrophages, and these immune cells trigger a cascade of cellular responses to regulate satellite cell activation, proliferation and differentiation.
-During this stage, we also see early fibroblast activity to form extra-cellular matrix.

Question 2

Muscle Prolifferation Phase

Answer 2

Day 4 -week 4
-Fibroblasts invade and take over extra-cellular matrix to stabilise tissue, anchoring to the fibrin and fibronectin derived from the blood of the haematoma to create a scaffold for new muscle fibres, and to build muscular connective tissue made of collagen
-Activation of satellite cells
-Satellite cells reproduce and differentiate into myoblasts which rebuild the muscular fibres
-There is some crossover into remodelling phase

Question 3

Muscle Remodelling phase

Answer 3

4 weeks to 4 months
-Disorganised (immature) muscle tissue is converted into organised (mature) muscle tissue
-Revascularisation and muscle innervation occur in the last stages of remodelling
*muscle innervation is suggested to be final stage

Question 4

Tendon haematoma/inflammatory phase

Answer 4

0-4 days
* -Initial healing after acute trauma begins with the formation of haematoma and a fibrin clot.
-The mechanical trauma causes a rupture of plasma membranes and the basal lamina, causing the cellular contents and chemotactic factors to empty into the extracellular space.
-This induces the infiltration of several types of immune cells, eg mast cells and neutrophils. As apoptosis occurs (necrosis of the fibres injured beyond repair), these phagocytes help to clear the damaged myofibres at the injury site (phagocytosis).
-During this stage, we also see early fibroblastic activity to form the extracellular matrix.

Question 5

tendon prolifferation

Answer 5

day 4 -6 weeks
-Fibroblasts continue to invade and take over the extracellular matrix, producing type 3 immature collagen and forming a ‘disorganised’ tendon callus
-They then lead the conversion of this type 3 (immature disorganised) collagen into type 1 (mature organised) collagen.

Question 6

tendon remodelling

Answer 6

6 weeks - 9 months
-Continued reorganisation and conversion of type 3 collagen into cross-linked organised type 1 collagen

Question 7

3 stages of tendinopathy

Answer 7

• Reactive tendinopathy:
  -Acute/abnormal compression or overload exceeds the capacity of what the tendon can handle
  -Results in short-term, adaptive thickening of a portion of the tendon
  -Tendon has potential to revert back if the overload is significantly reduced/there is significant time between loading sessions
• Tendon disrepair:
  -Further overload without adequate rest causes abnormal tenocyte proliferation, increased vascularity and neuronal growth (sensitises the area to pain), and collagen disorganisation
  -Some reversibility is possible with load management and exercise to stimulate the matrix structure
• Degenerative tendon:
  -Further vascularisation and collagen disruption
  -May be areas of acellularity and apoptosis
  -Thought that some changes are permanent/there is little capacity for reversibility of pathological changes at this stage