Soft Tissue Injury

Soft Tissue Injury

Tendon Injury

Three Mechanisms of Injury

(1) avulsion from bone – lose tendon insertion to bone (slow rate of load, e.g., football finger injury) – easier to repair

reattach with sutures, screws with spiked washers, or staples

(2) mid-substance tear – separation in middle of tendon (fast rate of load, e.g., rupture achilles tendon) – more common

(3) transection – slice tendon (e.g., knife wound)

Cellular Responses to Injury – involve fibroblasts and macrophages

intrinsic – cells from tendon itself (epitenon – around bundle of fibers, endotenon – between fibers)

extrinsic – cells from outside tendon – necessary if paratenon-uncovered (no sheath, e.g., achilles) or sheath injury

scar mass produced by broken sheath can produce problematic adhesions

long tendons have watershed areas with no vascular supply, requiring nutrients to diffuse long distances (achilles: 4 cm)

Three Stages of Repair

(1) Inflammatory – 3 days – phagocytes migrate in from nearby tissues, intrinsic or extrinsic fibroblasts activated

(2) Reparative – next 3 weeks – collagen is laid down and then resorbed and remodeled by monocytes

low tensile strength – use controlled passive range of motion exercises during this period, not active pulling

(3) Remodeling – next 3-4 weeks –fibroblasts align to long axis, cross-linkages are reestablished, and scar tissue forms

requires mechanical factors – collagen fiber orientation determined by tension of maturing granulation tissue

Biological Signaling Factors

PDGF – stimulates proliferation of fibroblasts (either intrinsic or extrinsic)

TGF-b – stimulates fibroblast migration/collagen synthesis

Clinical Repair – goal is to restore normal length

sutures must be aligned away from tendon gap and be strong enough to allow passive range of motion exercises
use passive motion to prevent extrinsic scar formation
however, active use is required for recovery of tensile strength and gliding function – prolonged immobilization not good

Ligament Injury – "sprain" – 25-40% of all knee injuries

Severity of Injury – three grades, depending upon extent of injury

(1) grade I – mild, no increased laxity so returns to normal length

(2) grade II – moderate, load exceeded peak tensile strength but no break – laxity, but firm end point, so still functional

(3) grade III – severe – complete disruption, no mechanical function (only 15% of knee injuries are grade III)

can be avulsion or mid-substance tear, depending upon rate of strain (see tendon mechanisms, above)
rarely, there will be a true failure at the ligament-bone junction – much easier to fix (length remains normal)

Three Stages of Repair – similar to tendon

(1) Inflammatory – 3 days – defect created by displacement and retraction filled with clot – signaling molecules influence this

acute inflammation begins with PMN’s; transition to monocytes occurs as fibroblasts invade and make matrix

(2) Reparative (Regeneration) – next 6 weeks – collagen matrix is produced by fibroblasts, then organized by monocytes

very cellular scar with fibroblasts and macrophages; also granulation tissue

(3) Remodeling – next 12 months –collagen III is aligned and replaced by collagen I; also decreased vascularity, fewer cells

ligament requires tension like tendons, but never returns to normal

Clinical Repair – suturing is useful only if ends are completely separated

immobilization – if necessary, must be very carefully timed; rehabilitation (e.g., swimming) is preferred

without movement, contraction limits joint motion – shortening due to mechanical, chemical, and electrical factors
also dramatic reduction in breaking strength, elastic stiffness, and strength of bone-ligament insertion
strength returns to normal after 4-12 months as bone remodels

ligament is difficult to repair if inside joint capsule, since synovial fluid inhibits healing – grafts are used instead

Articular Cartilage – common sports injury

Severity – depends upon depth of injury

(1) Superficial (collagen matrix is not disrupted) – chondrocytes will regenerate articular cartilage

(2) Superficial, disrupting matrix – very little repair, since chondrocytes do not de-differentiate

sometimes there will be transient increase in matrix component synthesis, but no new collagen matrix formed

(3) Penetrating subchondral bone (beyond tidemark) – more regeneration due to availability of stem cells/blood vessels

granulation tissue forms, matures into "hyaline-like" cartilage (<3 mm) or fibrocartilaginous tissue (>3 mm)

Clinical Repair – can use osteochondral grafts

immobilization – significant rapid loss of proteoglycans resulting in softening of cartilage and susceptibility to fibrillation