proximal to the injury. “with transection, axonal degeneration occurs, leaving the endoneural tubes of the last centimeter of the proximal stump occupied only by Schwann cells”.
– as a general rule, motor fibers are more susceptible to injury than sensory fibers, and large myelinated fibers are more susceptible than fine or nonmyelinated fibers.
– motor and sensory nerve fibers fail sequentially in the following order:
– pain – these are often the thinnest, nonmyelinated fibers, so it makes sense that they fail last.
– the order of recovery is then reversed (ie. pain returns first, then pinprick/temp, then proprioception, then motor).
– at the completion of regeneration, the surviving axon will be smaller than normal caliber and will be less thickly myelinated, and hence the conduction velocity will be less.
– the velocity of action potential propagation is DIRECTLY related to the diameter of the nerve – if the nerve is bigger, the faster the action potential will move.
– during depolarization, sodium rushes into the cell, potassium goes out; during repolarization, the sodium is pumped back out of the cell, the potassium is moved back in.
– myelin interferes with action potential initiation, but at the nodes of Ranvier there are high concentrations of voltage gated sodium channels – action potentials are evoked at the nodes and local currents flow quickly down the myelinated region to the next node. This salutatory conduction is a property of myelinated nerves.
– in the infant, the bones are filled with red marrow (hematopoeitic); this is replaced by yellow marrow beginning with the appendicular (peripheral) skeleton and later the axial skeleton. The process begins in the distal ends of the long bones and extends up to the proximal part – by age 20, only the upper end of the humerus and femur still contain red marrow.
– fibronectin is a ubiquitous serum and matrix protein that binds to a variety of common orthopaedic biomaterials, depending on the biomaterial’s composition. Bacteria can adhere to this fibronectin molecule – so the fibronectin has a role in promoting bacterial adherence to implants.
– reticulin is a scleroprotein from the connective fibers of reticular tissue – it is unlikely that it is found in tendons. Tendons probably do consist of elastin; they definitely have very straight, parallel collagen, and they have small concentrations of proteoglycan.
Tendon Healing in a Sheathed (avascular) tendon
– in the proper environment, the lacerated tendon itself is capable of repair – in repaired tendons treated with controlled passive motion, this “intrinsic” response, originating from the epitenon, predominates. In the immobilized tendon, healing occurs through the ingrowth of connective tissue from the digital sheath and cellular proliferation of the endotenon.
Tendon Healing in a paratenon covered (vascular) tendon
– wound fills up with inflammatory products and forms like a callus which remodels eventually
– laboratory parameters of DIC: increased fibrin split products (FDPs)
increased PT, PTT
decreased platelets (consumptive)
decreased antithrombin III (consumptive)
decreased fibrinogen (consumptive)
– in the meniscus, the concentration of proteoglycans and glycoproteins is only 10% that of hyaline cartilage.
– in the meniscus, the innervation is restricted to the peripheral 2/3rds.
– during stance phase, the foot is maximally dorsiflexed during midstance / terminal stance.
– the knee is maximally flexed at preswing
– the hip is maximally flexed at initial contact, maximally extended at terminal stance
Initial Contact Loading Response Midstance Terminal Stance Preswing
0% 0-10% 10-30% 30-50% 50-60%
Ankle 0 10 PF 5 DF 10 DF 20 PF
Knee 0 15 Flex 0 0 40 Flex
Hip 25 Flex 25 Flex 0 20 Ext 0
Ground reaction force
– Initial contact anterior to