11. Bone & Soft Tissue

Bone Structure & Function

• Periosteum: outer membrane covering bone surface; nourishes bone, provides anchorage for ligaments/muscles, contains nociceptors.
• Endosteum: membrane lining internal bone (medullary cavity, trabecular surfaces).
• Primary functions of bone
  • Support for red-marrow hematopoiesis.
  • Protect & support internal organs.
  • Endocrine secretion (hormones regulating mineral & energy metabolism – e.g., osteocalcin).
  • Mineral reservoir: Ca²⁺, P, amino acids, $HCO_3^-$.
  • Attachment sites for ligaments & muscles (leverage for movement).

Bone Composition

• Cortical (compact) bone
  • Tough, densely packed outer shell; surrounds trabecular bone.
  • ≈ $80\%$ of skeletal tissue; forms shafts (diaphyses).
• Trabecular (spongy) bone
  • Intermeshing thin plates (trabeculae) containing marrow.
  • ≈ $20\%$ of skeletal tissue; abundant in vertebrae, metaphyses, epiphyses.

Bone Remodeling Cellular Triad

• Osteoblasts (immature bone‐forming)
  • Deposit osteoid (collagen + matrix proteins) then mineralize it with Ca–P.
  • Net effect: absorption (bone formation).
• Osteoclasts (multinucleate resorbers)
  • Secrete acids & proteolytic enzymes → dissolve mineral + collagen.
  • Net effect: resorption.
• Osteoid: unmineralized collagenous matrix laid down by osteoblasts.

Fractures – General Concepts

• "Defect in continuity of bone"; 4 etiologic categories:
  • Traumatic (sudden impact)
  • Stress/Fatigue – repeated abnormal stress on normal bone.
  • Insufficiency – normal stress on weakened bone (↓ integrity).
  • Pathologic – fracture through diseased bone (tumor, infection, metabolic).

Stress/Fatigue Fractures

• Partial → pain with use; complete → true fracture line.
• High incidence: distance runners, military recruits.
• Locations: tibial shaft, metatarsals.
• Types:
  • Compressive – heel‐strike during prolonged march/run.
  • Distractive (avulsion) – muscle pull traction.

Vertebral Compression Fractures

• Progressive micro-fractures → vertebral body collapse.
• Causes: osteoporosis (most common), neoplasm, trauma.
• S/S: worsening back pain, ↓ mobility, gait dysfunction, paresthesia, postural kyphosis.

Insufficiency Fractures

• Occur in bone with ↓ elastic resistance or mineralization (post-radiation, corticosteroid-induced, metabolic disease, postmenopause).

Pathologic & Epiphyseal Fractures

• Pathologic: fragile bone due to disease/neoplasm.
• Epiphyseal: growth-plate injuries in children/adolescents (Salter–Harris).

Descriptive Classifications (Any Etiology)

• Open (compound) vs. Closed – skin integrity.
• Complete vs. Incomplete – entire cortex broken?
• Displaced vs. Nondisplaced – alignment.
• Comminuted – >2 fragments.
• Line pattern: Transverse (shear), Oblique, Spiral (torsion), Segmental, Avulsed, Impacted, Torus (buckle), Greenstick (children).

Stages of Fracture Healing (Sheen & Garla, 2019)

1. Hematoma/Early Inflammation (Days 1–5)
   • Torn vessels → hematoma.
   • Clot seals ends; bone cells die; inflammatory cascade begins.
2. Fibrocartilaginous Callus (Days 5–11)
   • Phagocytosis debris; angiogenesis.
   • Fibroblasts lay collagen; chondroblasts form soft hyaline cartilage callus.
   • Osteoblasts begin spongy bone.
3. Bony (Hard) Callus / Endochondral Ossification (Days 11–28)
   • Chondroclasts resorb cartilage, osteoblasts deposit woven bone → hard callus.
4. Remodeling (Day 18 → months/years)
   • Osteoclast–osteoblast coupling restores medullary cavity & original contour responding to Wolff’s law.

Healing timelines (avg):

• Children $4!−!6$ weeks; Adolescents $6!−!8$ weeks; Adults $10!−!18$ weeks.
• Influencers: fracture type/site, vascularity, systemic health, age, activity level, concurrent injuries.

Metabolic Bone Disorders – Overview

• Osteoporosis – ↓ density.
• Osteomalacia – softening from poor mineralization.
• Paget Disease (Osteitis Deformans) – disordered remodeling.
• Also: Osteopenia (low mass) & Osteopetrosis (↑ density).

Osteoporosis

• Chronic, progressive; ↓ bone mass & quality → fragility ↑ fracture risk.
• Affects >10 million in US; prevalence rising with aging.
• Most common metabolic bone disease; underdiagnosed in men.

Types

• Primary (most common): post-menopausal women, elderly men.
• Secondary: drugs (corticosteroids, heparin, anticonvulsants), EtOH, malnutrition/malabsorption, endocrine disorders, prolonged immobilization, etc.

Etiology & Pathogenesis

• Prolonged negative Ca²⁺ balance, ↓ androgens/estrogens (↑ osteoclasts ↓ osteoblasts), sedentary lifestyle.
• Rate: osteoclastic resorption > osteoblastic formation; altered apoptosis.
• Bone becomes porous, brittle.

Risk Factors

• Age (postmenopausal, >65 y), white/Asian women, thin body habitus, family Hx, inactivity, low Ca/D₃, drugs (heparin, corticosteroids), psychological stress, smoking, EtOH.

Clinical Manifestations

• Height loss, kyphosis/dowager’s hump, back pain, fractures (vertebrae, hip, ribs, distal radius, femur), compression fractures → severe pain.

Diagnosis / Screening

• H&P, labs, imaging.
• Dual-energy X-ray absorptiometry (DXA) – BMD expressed as T-score/Z-score.
  • Normal: $\geq −1.0$ SD.
  • Osteopenia: $−1.0 \text{ to } −2.5$ SD.
  • Osteoporosis: < −2.5 SD.

Medical Management

• Optimize peak BMD by age ≈30.
• Lifestyle: Ca (see RDA table), Vit D, diet, weight-bearing/resistance exercise.
• Pharmacology
  • Bisphosphonates (Fosamax, Boniva PO/IV, Actonel, Reclast) – first-line.
  • SERMs (Raloxifene/Evista) – estrogen receptor modulation.
  • Anabolic PTH analog Teriparatide (Forteo) – up to 2 yrs.
  • RANK-L antibody Denosumab (Prolia) – twice yearly.
  • Calcitonin nasal/inj (oldest; compression fx pain).
  • Romosozumab (Evenity, 2019) – sclerostin inhibitor, 12 monthly doses.

Physical Therapy Guidelines

• Weight-bearing 3–5 ×/wk (prefer 5–7).
• Resistance 2 ×/wk.
• Endurance (walk, stair, etc.) 30–60 min most days.
• Balance, posture re-education, fall prevention, patient education.

Osteomalacia (Adult Rickets)

• Progressive softening from deficient mineralization of osteoid (↓ Ca, Vit D, or PO₄).
• Rare in U.S.

Major Etiologies

1. Insufficient intestinal Ca absorption – dietary lack or Vit D resistance.
2. ↑ Renal PO₄ wasting – renal osteodystrophy, renal tubular acidosis causing hypophosphatemia.

• Others (Box 24-6): antiepileptics, malnutrition, tumors producing FGF-23, etc.

Pathogenesis

• Osteoid produced but fails to calcify → ↑ uncalcified matrix; bone architecture intact yet mechanically weak.

Clinical Manifestations

• Diffuse bone pain/tenderness (spine, ribs, pelvis, proximal limbs), muscular weakness & weight loss, bowing of legs, kyphosis, fracture susceptibility, polyneuropathy, ataxia, ↑ fall risk.

Diagnosis & Treatment

• Imaging (X-ray – Looser’s zones), bone scan, biopsy, labs (↓ Ca, ↓ PO₄, ↑ alkaline phosphatase).
• Supplement Ca/Vit D; phosphate replacement; manage renal issues. Deformities often irreversible.
• PT: strength, ROM, posture, balance, compliance.

Paget Disease (Osteitis Deformans)

• 2nd most common metabolic bone disorder.
• Excessive, disorganized bone remodeling: ↑ osteoclastic resorption → ↑ unstructured osteoblastic deposition → dense but weak bone.
• Common sites: pelvis, femur/tibia, skull, lumbar spine.

Etiology

• Unknown; risk ↑ after 40 y, M>F, Anglo-Saxon heritage, familial autosomal-dominant variants (genes regulating osteoclast differentiation), possible measles/viral triggers.

Pathogenesis Phases

1. Resorptive – rapid osteoclastic lysis replaced by fibrous tissue.
2. Sclerotic (mixed) – haphazard thick trabeculae + irregular cortical thickening.

Clinical Manifestations

• Often asymptomatic (70 %).
• Bone pain, deformity (bowing femur/tibia, thoracic kyphosis, enlarged skull), fractures, OA, neurologic (pagetic steal → spinal/cranial nerve ischemia), CV high-output failure due to bone/skin vasodilation, ↑ osteogenic sarcoma risk (~1 %).

Diagnosis & Management

• ↑ Serum alkaline phosphatase; imaging (X-ray, bone scan), biopsy.
• Bisphosphonates (IV/oral) mainstay; pain meds.
• PT: strength/stretching, weight-bearing (avoid jogging/impact/bend/twist); educate.
• Prognosis good if treated before major deformity; biochemical remission common.

Soft Tissue & Joint Disorders

Strains (Muscle–Tendon Unit)

• Mechanism: overstretch/overwork, eccentrics, crossing 2 joints.
• Grades:
  • I (mild): minor swelling, no strength loss.
  • II (mod): partial tear, pain, edema, ↓ ROM/force.
  • III (severe): complete rupture; surgery.
• Symptoms: delayed soreness (≈24 h), tenderness, spasm, edema, stiffness.

Sprains (Ligament Injury)

• Etiology: abnormal stress/tear; ankle inversion common.
• Ligament functions: stability, proprioception, bone positioning.
• Grades:
  • I : micro-tear, no instability.
  • II: partial tear, moderate instability/pain.
  • III: full rupture, gross laxity, minimal initial pain (nerve torn); surgery/immobilization.

Dislocation vs. Subluxation

• Dislocation: complete loss of joint congruity (GHJ most common) → severe soft-tissue damage.
• Subluxation: partial loss; contact maintained. Manage muscle imbalance, adjacent hypomobility.

Tendon Injuries & Tendinopathy

• Mechanisms: rapid high tension, compression, friction; fluoroquinolone antibiotics ↑ risk (esp. transplants, corticosteroid use).
• Terminology: Tendinopathy (chronic), Tenosynovitis (sheath), Tendinosis (degeneration > inflammation).

Synovitis & Other Soft-Tissue Lesions

• Synovitis: inflamed synovial membrane → effusion.
• Hemarthrosis: bleeding into joint (trauma, hemophilia).
• Ganglion cyst: ballooned capsule/tendon wall.
• Bursitis: inflamed bursa (friction cushion).
• Overuse Syndrome: cumulative microtrauma → inflammation/pain.
• Muscle Weakness: neurogenic, myopathic, disuse.
• Contracture: adaptive shortening; Adhesions: collagen crosslinks restricting glide.

Myofascial Compartment Syndromes (MCS)

• Compartment: muscle + NV bundle enclosed by non-yielding fascia.
• Pressure ↑ → compromised perfusion & neuroconduction.
• Leg (anterior) most common.

Etiologic/Predisposing Factors

• Fracture, contusion, crush, burns, reperfusion after ischemia, restrictive casts/dressings, excessive exercise, snake bite, gunshot.

Acute Compartment Syndrome (ACS)

• Trauma onset within hours (≤48 h). Surgical emergency (fasciotomy).
• S/S: severe disproportionate pain, pain on passive stretch, not relieved by analgesics; paresthesia, tense shiny skin, ↓/absent pulse, paresis/paralysis.

Chronic (Exertional) Compartment Syndrome

• Runners, military; anterior/lateral leg; precipitated by footwear/surface/over-training.
• "5 P’s": Pain/cramp, Pulselessness (often subtle), Paresthesia, Paresis, Pallor; worsen with activity, subside with rest.

Complications

• Untreated → ischemia, irreversible muscle/nerve loss, scarring, disability, amputation.

PT Role

• Post-op: prevent immobilization effects, flexibility/strength, control inflammation, graded strengthening, scar mgmt, education.

Heterotopic Ossification (HO)

• Benign bone in nonosseous tissue (muscle, fascia).
• Myositis ossificans: HO within bruised muscle.
• Neurogenic HO: post-SCI/TBI.
• Highest after THA; sites: hip>elbow>shoulder>knee.

Etiology

• Trauma: fractures, surgeries, SCI (below lesion), TBI, burns, amputations; military blast ↑ incidence; severity correlates.
• Hereditary forms: fibrodysplasia ossificans progressiva, etc.

Clinical Presentation

• Pain & ↓ ROM within 2 wks post-injury; hallmark = progressive motion loss w/ rigid end-feel; can ankylose joint; ulnar nerve entrapment at elbow.

Management

• NSAIDs, bisphosphonates, low-dose radiation (prevent calcification), surgical excision after maturity.
• Rehab: ROM restoration, dynamic splinting, function; avoid aggressive stretching early.

Myopathies

• Umbrella: muscle diseases causing nonspecific weakness.
• Acquired: inflammatory (dermato/polymyositis), endocrine, drug-induced (statins), critical illness myopathy.
• Hereditary: muscular dystrophies, metabolic (glycogen, lipid), mitochondrial.

Idiopathic Inflammatory Myopathies (Myositis)

• Immune-mediated; environment triggers genetically susceptible host.

Critical Illness Myopathy (CIM)

• Prolonged ICU stay; fiber atrophy, fatty degeneration, fibrosis → profound weakness.

Diagnosis

• Clinical exam, MMT, EMG, US, MRI, genetic tests, muscle biopsy.

Clinical Features

• Progressive proximal weakness, pain/tenderness, fatigue, ↓ endurance/coordination/aerobic capacity → functional loss.

Physical Therapy

• Tailor to type & stage; acute inflammation → rest & PROM; progress to isometrics, low-intensity isotonic/aerobic, aquatics, breathing; monitor fatigue, use ADs; education.

Myofascial Pain Syndrome (MPS)

• Chronic regional pain with myofascial trigger points (TrP) in taut band.
• Active TrP: spontaneous local + referred pain, reproduces familiar pattern; painful at rest/with use.
• Latent TrP: silent unless palpated, but can restrict ROM.

Pathogenesis & Causes

• Dysfunctional shortened sarcomeres & endplate hyperactivity; inflammatory mediators.
• Contributors: chronic overload (repetitive/maintained shortening), acute overload (slip/lift trauma), deconditioning, poor posture, leg-length discrepancy, bad ergonomics, central sensitization.

Clinical Manifestations

• Dull, deep, aching pain; cold sensation; paresthesia; restricted ROM, ↓ strength; specific referred patterns; autonomic signs.

PT Management

• Identify biomechanics, inactivate TrP (manual pressure, dry needling, modalities), stretching, ROM, muscle re-education, sustained home stretching & exercise.

Osteoarthritis (OA)

• Most prevalent musculoskeletal disorder; major indication for arthroplasty.
• Irreversible degenerative disease of entire synovial joint (cartilage, bone, menisci, ligs, capsule).

Epidemiology & Risk Factors

• Risk: age, obesity, female, muscle weakness, laxity, prior injury, anatomic malalignment, genetics, high-intensity sports, smoking (knee severity), occupational loading.

Pathogenesis

• Progressive cartilage erosion → subchondral sclerosis, cysts, osteophytes; mild synovitis; joint space narrowing; pain due to bone, synovium, ligaments.

Clinical Features

• Gradual pain with activity, crepitus, ↓ ROM, tenderness, malalignment (varus), morning stiffness <30 min, Heberden’s (DIP) & Bouchard’s (PIP) nodes, later deformity.
• Radiology progression: early joint-space widening, then sclerosis, cysts, osteophytes, narrowing.

PT Implications

• Exercise × joint protection: isometric/strength, aerobic, gait training; reduces pain, improves function, delays surgery; patient education.

Rheumatoid Arthritis (RA)

• Chronic systemic autoimmune polyarthritis; symmetrical.
• Extra-articular: CV, pulmonary, GI, ocular, neuro, osteoporosis.

Etiology & Pathogenesis

• Autoimmunity with genetic predisposition (HLA-DR), environmental triggers.
• Infiltration of T/B, macrophages → synovitis → synovial hyperplasia, angiogenesis.
• Formation of pannus – granulation tissue eroding cartilage & bone.

Systemic Involvement

• Pulmonary (pleuritis, nodules), CV (premature CAD, pericarditis), Neuro (cervical myelopathy), Musculoskeletal (myopathy), ↑ infections.

Joint Deformities

• Swan-neck: PIP hyperextension + DIP flexion.
• Boutonnière: PIP flexion + DIP hyperextension.

Management

• Medications: NSAIDs, DMARDs, biologics (cytokine blockers).
• PT goals (Ottawa Panel): ↓ pain/swelling, correct deformity, ↑ ROM/strength/fitness/function, ↓ fatigue.

Comparative Summary – OA vs. RA

• Onset: OA gradual (>40 y, peak >65); RA 25–50 y, acute–subacute flares/remission.
• Incidence: OA ~12 % adults; RA 1–2 %.
• Gender: OA – men earlier, women later; RA – 3× women (severe in men).
• Etiology: OA multifactorial mechanical/degenerative; RA autoimmune.
• Disease Process: OA chronic degeneration, usually unilateral bigger joints; inflammation mild; pain ↑ with movement.
• RA systemic inflammatory; symmetric small & large joints; pain ↓ with gentle movement.
• Systemic S/S: None in OA; fatigue, malaise, wt loss, fever in RA.

Ethical, Practical, & Real-World Implications

• Early screening (DXA) vital; health professionals must educate sedentary aging population.
• Polypharmacy (bisphosphonates, biologics) requires fall & side-effect monitoring.
• PT role crucial across spectrum: fracture rehab, fall prevention, strength/balance programs, ergonomic advice, chronic disease management.
• Equity considerations: men under-diagnosed with osteoporosis; minority access to DXA/therapy; cost of biologics.