Reaction_of_Musculoskeletal_Tissues_to_Disorders_and_Injuries.pptx

reaction

1. Reaction of Musculoskeletal Tissues to Disorders and Injuries dr. Yudha Mathan Sakti, Sp. OT (K) Orthopaedics & Traumatology Gadjah Mada University

2. Reactions of Bone

3. Reactions of bone Local death (avascular necrosis) Alteration of bone deposition Increased deposition Decreased deposition Alteration of bone resorption Increased resorption Decreased resorption Mechanical failure/fracture Increase radiographic density  sclerosis Decrease radiographic density  rarefaction

4. Local Death When an area of bone is completely deprived of its blood supply  avascular necrosis of bone T he resultant segment of dead bone then becomes an abnormal condition  Incites further reactions from surrounding living tissues.

5. Reaction of living bones Altered deposition of bone Increased deposition (↑ matrix formation, normal calcification) Decreased deposition (either ↓ matrix formation or ↓ calcification) Altered resorption of bone Increased resorption Decreased resorption Combination of altered deposition and altered resorption Reactions can be: Localized (bone as a structure) Generalized (all bones as an organ)

6. Bone as an Organ (Generalized) Deposition > resorption Osteopetrosis / Marble bones Acromegaly Resorption > depostion Osteopenia & Osteoporosis Osteogenesis imperfecta Rickets in children Osteomalacia in adults

7. Bone Deposition > Bone Resorption ( Generalized increase in bone) Normal deposition, ↓ resorption. Exessive intramembranous ossification from periosteum (↑ bone deposition) Osteopetrosis (Marble bones) Acromegaly

8. Bone Deposition < Bone Resorption ( Generalized decrease in bone) ↓ osteoblastic formation, ↑ resorption examples: congenital osteogenesis imperfecta, disuse osteoporosis, steroid-induced osteoporosis, postmenopausal osteoprosis Normal matrix formation, ↓ calcification Osteoporosis (osteopenia) Rickets (children) & Osteomalacia (adults)

9. Bone as a structure (Localized) Deposition > resorption Work hypertrophy (Wolff’s law) Degenerative OA Fractures (Callus) Infection (Caused by Pus) Osteosclerosic neoplasm Reactive bone Reaction of ↑ deposition to certain benign neoplasm & neoplasmlike lesions (osteoid osteoma) Tumor bone Bone produced by certain malignant neoplasm (osteosarcoma & osteoblastic mestastases)

10. Bone as a structure (Localized) Resorption > depostion Disuse atrophy / disuse osteoporosis Rheumatoid arthritis Periarticular soft tissue inflammation  d e position ↓, resorption ↑ Infection Local destruction/resorption of bone (osteolysis)  periosteum react by new bone deposition (outside of the bone) Osteolytic neoplasm

11. Mechanical failure/Fracture: Fracture : discontinuity of a bone’s structure, partially or completely, due to failure to withstand force Tough collagen fibers  tensile strength Calcified inorganic matrix  compressive strength In children  bone is elastic, less stress may bend the bone  plastic deformation of bone caused by less severe force

12. Reactions of Epiphyseal Plate

13. Reactions of Epiphyseal Plates Three basic ways epiphyseal plates can react : Increased growth Decreased growth Torsional growth Normal growth requires intact plate structure, normal blood supply (comes in from peiphyseal side of the plate), and intermittent pressures with normal activities.

14. Reactions of Epiphyseal Plates Injury  part, or all of it to close (ossify)  stops growth Prolonged hyperemia  stimulates growth Relative ischemia  retards growth Complete ischemia  necrosis  stops growth Excessive continuous pressure on the plate  retards growth Decrease in normal intermittent pressure (occurs in decreased function of a limb)  retards growth Stimulation / retardation occurs in one part of an epiphyseal plate, while normal growth continues on the remainder  uneven growth  angulatory deformity

15. Generalized reaction Increased growth (Gigantism) Arachnodactily ( Hyperchondroplasia / Marfan’s syndrome) Pituitary Gigantism Decreased growth (Dwarfism) Achondroplasia Pituitary dwarfism (Lorain type) Rickets

16. Localized increase in growth Increased growth Chronic inflammation Prolonged hyperemia  local growth Displaced fracture of the shaft of a long bone Disrupted nutrient supply  temporary compensantory hyperemia  temporary local growth Congenital arteriovenous malformations Continuous hyperemia  overgrowth

17. Localized decrease in growth Disuse retardation Prolonged immobilization / relief of weightbearing / severe paralysis  ↓ pressure  local growth ↓ Physical injury Fracture that crosses or crushes the plate  bony union  local growth ↓ Thermal injury Frosbite / burns  destroys plate Ischemia Total avascular necrosis of epiphysis  necrosis of cartilage in plate Infection Pus (esp. Caused by Staphylococcus )  chondrolytic  partial destruction  uneven growth

18. Localized torsional growth When growing long bone are subjected to continual / intermittent twisting forces (ex: postural habits sitting on the floor)  Bone gradually becomes twisted in same direction force applied. Can usually be reversed  corrective torsional forces in opposite direction. Educating the patient to change habits.

19. Reactions of Synovial Joint

20. Reactions of synovial joints Normal joint  smooth cartilage surface  painless and frictionless movement Joint capsule is sensitive to increased pressure (by fluid -- effusion) / stretching Articular cartilage  produces proteoglycans and collagen, that is stimulated by cyclical pressure that transmitted by the matrix

21. Destruction of articular cartilage RA Infection Ankylosing spondylitis Prolonged immobilization of a synovial joint Continuous compression of articular cartilage Intra-articular injections of hydrocortisone (hydrocortisone arthropathy )

22. Degeneration of articular cartilage Premature aging of cartilage (wear and tear) Previous destruction of cartilage Incongruity / irregularity of joint surfaces Peripheral proliferation Composed of cartilage (chondrophyte formation) Subsequently ossifies ( osteophyte formation )  peripheral ring / lip

23. Healing and regeneration Possibility  CPM (continuous passive motion) would stimulate the healing & regeneration of articular cartilage Through differentiation of pluripotential mesenchyme cells in subchondral bone.

24. Reactions of synovial membrane Effusion (produce of excessive amount of fluid) Serous – mild sprain Exudate – Synovitis, RA Purulent – Septic athritis Hemorrhagic – severe injury, hemophilia Hypertrophy (thicker) Adhesion – Prolonged immobilization (cast/rigid splint)

25. Reactions of joint capsule and ligaments Joint laxity (unduly stretch & elongated) – joint instability Joint contracture (tight & shortened) – limited ROM Joint contracture, caused by: Congenital – clubfeet Infection – fibrosis & scar formation Chronic arthritis – RA & joint degeneration Muscle contracture – Ischemic contracture, 2 nd to compartment syndrome; muscle imbalance; prolonged muscle spasm Joint laxity, caused by: Genetically – generalized Injury – dislocation, subluxation, rupture Infection – Septic arthritis

26. Reactions of skeletal muscle Disuse atrophy Work hypertrophy Ischemic necrosis Contracture Regeneration

27. Disuse atrophy Unused muscle  weaker and smaller Poliomyelitis (anterior horn cell) Polyneuritis (peripheral nerve fiber) Myasthenia gravis ( myoneural junction) Muscular dystrophy (Individual muscle fiber) Prolonged immobilization

28. Types of Bony Deformities

29. Work hypertrophy : isometric contraction – enlargement of muscle fiber Ischemic necrosis : within 6 hours Contracture  Persistent shortening, resistant to stretching  Muscular dystrophy, Cerebral palsy Regeneration from sarcolemma, satellite cell in each fiber

30. Musculoskeletal deformities

31. Bony deformity Types: Loss of alignment Abnormal length Bony outgrowth Causes: Congenital Fracture Disturbances of epiphyseal plate growth Bending of abnormality soft bone Overgrowth adult bone

32. Joint deformity Types: Displacement of the joint Completely: luxated Partially: subluxated, dislocated Excessive mobility (hypermobility) of joint Restricted mobility of joint

33. Joint deformity Causes: Congenital – DDH/developmental dysplasia of the hip, clubfeet, radioulnar synostosis Acquired dislocation – traumatic, pathological Mechanical blocks – OA, displaced intraarticular fracture Joint adhesions – RA, septic arthritis Muscle contractures Muscle imbalance – spastic, flaccid Fibrous contracture of fascia & skin – burns, dupuytren’s External pressure – pointed shoe  hallux valgus Idiopathic – scoliosis

34. Take Home Message A surgeon must know how the musculoskeletal system reacts towards changes that happens within or around it to determine course of treatment based on what’s best for the patient in long term By understanding the basics, we should be able to educate patients better on their condition

35. Thank you