Review of musculoskeletal system
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Review of Musculoskeletal System. Chapter 36. Skeletal System. Function: Protection Hematopoiesis Mineral homeostasis Calcium Phosphorus Carbonate Magnesium. Structure. Bone is a connective tissue: Matrix Collagen fibers for flexibility and tensile strength Calcium for rigidity

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Skeletal system l.jpg
Skeletal System

  • Function:

    • Protection

    • Hematopoiesis

    • Mineral homeostasis

      • Calcium

      • Phosphorus

      • Carbonate

      • Magnesium

Structure l.jpg

  • Bone is a connective tissue:

    • Matrix

      • Collagen fibers for flexibility and tensile strength

      • Calcium for rigidity

      • Hydroxyapatite Ca5(PO4)3OH

Slide4 l.jpg

  • Cells:

    • Osteoblast

      • Form organic components of matrix

    • Osteocyte

    • Osteoblasts

      • From monocytes

      • Secrete citric and lactic acids

      • Collagenases and other enzymes

      • Stimulated by PTH

      • Inhibited by Calcitonin

Types of bone l.jpg
Types of Bone

  • Dense or Compact (85%)

    • Osteon (Haversian System)

    • Central (Haversian) canal

    • Lamellae

    • Lacunae with osteocytes

    • Canaliculi

  • Spongy (cancellous) bone (15%)

    • trabeculae

Periosteum l.jpg

  • Outer layer is dense, irregular CT with nerves and blood vessels

  • Inner layer

    • Osteoblasts

    • Anchored to bone by collagen fibers that penetrate into bone

Bone formation l.jpg
Bone Formation

  • Endochondral ossification

    • Inside hyaline cartilage

    • Most bones

  • Intramembranous ossification

    • Forms directly inside membranes

    • Bones of skull

Growth l.jpg

  • Lengthening of bones at epiphyseal plate

    • Grows from cartilage

  • Forms epiphyseal line when done growing

  • Undergoing constant remodeling

    • Adaptation to stress

    • Healing

Skeleton l.jpg

  • 206 bones

  • Axial skeleton

    • Skull and hyoid

    • Vertebral column

    • Ribs and sternum

  • Appendicular skeleton

    • Shoulder girdle

    • Pelvic girdle

Classification l.jpg

  • Long bones:

    • Diaphysis

    • Epiphysis

    • Metaphysis

    • Medullary cavity

    • Endosteum

Classification cont l.jpg
Classification cont.

  • Short bones

  • Flat bones

  • Irregular bones

  • Sesamoid bones

  • Wormian bones

Joints l.jpg

  • Degree of movement

    • Synarthrosis – immovable joint

    • Amphiarthrosis – slightly movable joint

    • Diarthrosis – freely movable joint

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  • Synovial joints

    • Joint capsule

      • Fibrous CT

      • Tendons and ligaments

      • Nerves, blood and lymph vessels

    • Synovial membrane

      • Loose fibrous CT

      • Many blood vessels – good repair

    • Joint (synovial) Cavity

Slide25 l.jpg

  • Synovial fluid

    • Plasma filtrate

    • Synovial cells and leukocytes phagocytize debris and microbes

  • Articular cartilage

    • Reduce friction

    • Distribute force

Bone pathophysiology l.jpg
Bone Pathophysiology

  • Inherited conditions:

    • Osteogenesis imperfecta

      • Inherited defect in collagen synthesis

      • Osteopenia and brittle bones

      • Often- defective tooth formation, blue sclera, faulty hearing

      • Inheritance can be dominant, recessive or by new mutation

      • Several degrees of severity

Slide28 l.jpg

  • Achondroplasia

    • Involves a defect in normal cartilage development

    • Epiphyseal plates close early in long bones; individual has short arms and legs, but normal spine and skull

    • Dominant inheritance, but frequent new mutations

    • Other organs develop normally

    • Individuals live a normal lifespan

Acquired disorders l.jpg
Acquired disorders

  • Osteoporosis – “porous bone”

    • Most common metabolic bone disease in North America

    • Can be attributed to genetics, diet or hormones

    • Most osteoporosis is idiopathic osteoporosis

    • Bone loss due to an identifiable cause is secondary osteoporosis

    • Bone tissue is mineralized normally, but over time the structural integrity of bone is lost and it becomes thinner and weaker, and more prone to fractures.

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  • Key features: bone fracture and the associated pain.

  • WHO defines osteoporosis by bone density:

    • Normal bone > 833 mg/cm2

    • Osteopenia 833 to 648 mg/cm2

    • Osteoporosis < 648 mg/cm2

  • Can be generalized, involving major portions of the axial skeleton

  • Can be regional, involving one segment of the appendicular skeleton

Slide32 l.jpg

  • Remodeling is constant

    • Teen years more bone is laid down than reabsorbed

    • Peak bone mass or maximum density reached at around 30 years of age

    • After age 30, bone is reabsorbed faster than it is laid down

    • In women, bone loss is most rapid in the first years after menopause, but continues throughout postmenopausal years

    • Est. 55% of people over 50 have osteoporosis or low bone mass.

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  • Men also lose bone density, but start out with more bone mass so takes longer.

  • By age 90 about 17% of males have had a hip fracture, vs. 32 % of females

  • Vertebral fractures also occur → kyphosis

  • Most common in whites, but affects all races.

  • African Americans have about half the fracture rates of whites (higher peak bone mass)

Risk factors l.jpg
Risk factors mass so takes longer.

  • Family history

  • White race

  • Increased age

  • Female sex

  • Small stature

  • Fair or pale skin

  • Thin build

  • Early menopause (natural or surgical)

  • Late menarche

Risk factors cont l.jpg
Risk factors cont. mass so takes longer.

  • Nulliparity

  • Obesity

  • Weight below a healthy range

  • Acidosis

  • Low dietary calcium and vitamin D

  • High caffeine intake

  • Sedentary life style

  • Smoker

  • Excessive alcohol consumption

  • Liver, kidney disease, rheumatoid arthritis, etc.

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  • Often progresses silently for decades until fracture occurs mass so takes longer.

  • Bones can fracture spontaneously

  • Most severe in spine, wrist and hips

  • Estrogens and androgens may be factors in both sexes

    • Testosterone is converted into estrogen in peripheral tissues and decreases bone loss

  • Rapid bone loss is osteoclast mediated

  • Slow bone loss is osteoblast mediated

Clinical manifestations l.jpg
Clinical manifestations mass so takes longer.

  • Pain and bone deformity

  • Kyphosis caused by vertebral collapse

  • Fractures of long bones

  • Fatal complications include fat or pulmonary embolism, pneumonia, hemorrhage and shock

  • 20 % die as a result of surgical complications

Treatment l.jpg
Treatment mass so takes longer.

  • No known cure

  • Slow bone loss and promote bone deposition

  • Calcium and vitamin D supplements

  • Calcitonin

  • Hormone replacement therapy

  • Biophosphates – inhibit osteoclasts

  • Dual x-ray absorptiometry for diagnosis


Prevention l.jpg
Prevention mass so takes longer.

  • Intake of calcium, vitamin D, magnesium and possibly boron

  • Regular, weight-bearing exercise

  • Avoid tobacco and glucocorticoids

  • No alcoholism

  • Hormone replacement?

  • Parathyroid hormone?

  • Testosterone for men and possibly women

Rickets and osteomalacia l.jpg
Rickets and Osteomalacia mass so takes longer.

  • Inadequate mineral deposition in essentially normal organic matrix

  • Softened bone:

    • Subject to malformation and distortion –pain

Rickets l.jpg
Rickets mass so takes longer.

  • Dietary vitamin D deficiency causes inadequate mineralization of the developing skeleton in infants and children

  • Rarely seen in Western nations

    • Poverty

    • Ignorance

  • Bones are soft and easily deformed

  • Tendency to fractures

  • Therapy: supply vitamin D and calcium

Osteomalacia l.jpg
Osteomalacia mass so takes longer.

  • Rarely due to vitamin D deficiency

  • Usually GI malabsorption, renal defect or chronic kidney or liver diseases.

  • Elderly often affected due to inadequate diet or lack of outdoor activity

  • May accompany and complicate osteoporosis.

Joint disorders l.jpg
Joint Disorders mass so takes longer.

  • Osteoarthritis

    • Most common joint disease in North America

    • Minimal inflammatory component

    • Differentiated from inflammatory disease by:

      • Absence of synovial membrane inflammation

      • Lack of systemic signs and symptoms

      • Normal synovial fluid

    • Much of the pain and loss of mobility associated with aging.

Osteoarthritis l.jpg
Osteoarthritis mass so takes longer.

  • Incidence increases with age: 85% of people age 65 have some joint degeneration

  • Incidence similar, but women more severely affected

  • Exceptional stress on joints: gymnasts, etc.

  • Biochemical defect in cartilage

  • Malformed joint, obesity and postural defects

  • Genetic component

  • Torn ACL or meniscectomy

Osteoarthritis48 l.jpg
Osteoarthritis mass so takes longer.

  • When associated with known risk factors it is secondary OA

  • No risk factors – idiopathic OA

  • Pathological characteristics:

    • Erosion of the articular cartilage

    • Sclerosis of subchondral bone

    • Formation of bone spurs or osteophytes

Osteoarthritis49 l.jpg
Osteoarthritis mass so takes longer.

  • Begins in articular cartilage

    • Yellow-grey or brownish gray

    • Thin, irregular, frayed

    • Cracks or fissures develop (fibrillation)

    • Fluid filled cysts may form

    • Microfractures of subchondral bone

    • Formation of fibrocartilage repair plugs

    • Bone surface exposed

    • Bone responds by becoming dense and hard

Osteoarthritis50 l.jpg
Osteoarthritis mass so takes longer.

  • Synovial membrane is indirectly affected

    • Fragments of fibrocartilage cause inflammation –pain

    • Fibrous repair of joint capsule restricts motion

    • Osteophytes form – pain and loss of motion

      • Joint mice

Osteoarthritis51 l.jpg
Osteoarthritis mass so takes longer.

  • Affects one or more weight-bearing joints

    • Hand, wrist, lower cervical spine, lumbar spine and sacroiliac, hip, knees, ankles, feet

  • Aches and stiffness

    • Symptoms increase with activity; diminish with rest

  • Usually no swelling or redness of adjacent tissues

  • Sometimes nocturnal pain – may be referred

Osteoarthritis52 l.jpg
Osteoarthritis mass so takes longer.

Primary signs and symptoms of joint disease are:

pain, stiffness, enlargement or swelling, tenderness, limited range of motion, muscle wasting, partial dislocation, and deformity

Osteoarthritis53 l.jpg
Osteoarthritis mass so takes longer.

  • Evaluation made through clinical assessment and radiologic studies, CT scan, arthroscopy and MRI

  • Treatment:

  • Glucosamine may decrease pain and slow or stop progression – 1500 mg/day

  • Chondroitin sulfate – questionable absorption

Osteoarthritis54 l.jpg
Osteoarthritis mass so takes longer.

  • Analgesics and antiinflammatory drugs

  • Range of motion exercises

  • Reduce aggravating factors

    • Weight loss

    • Use of cane, crutches or walker

  • Surgical removal of bone spurs

  • Replacement of joint

Rheumatoid arthritis l.jpg
Rheumatoid Arthritis mass so takes longer.

  • Systemic disease with prominent involvement of the joints

  • Inflammatory joint disease characterized by:

    • Inflammatory damage in the synovial membrane or articular cartilage

    • Systemic signs of inflammation: fever, leukocytosis, malaise, anorexia, hyperfibrinogenemia)

Rheumatoid arthritis56 l.jpg
Rheumatoid Arthritis mass so takes longer.

  • Systemic autoimmune disease that causes chronic inflammation of connective tissue

  • Initially affects synovial membrane

  • Later articular cartilage, joint capsule, ligaments and tendons, and bone

  • Affects joints of hands, wrists, ankles, and feet, but shoulders, hips and cervical spine may also be involved

  • Systemic effects on heart, kidney, lungs, skin and other organs

Rheumatoid arthritis57 l.jpg
Rheumatoid Arthritis mass so takes longer.

  • Mild to severe

  • Destroys and distorts joints

  • Reduces life expectancy

  • Remission and exacerbation

  • 1 – 2% of adult population

  • Women : men = 3:1

  • Onset usually in 20’s or 30’s

  • Symptoms lessen during pregnancy

  • Seasonal variation

Rheumatoid arthritis58 l.jpg
Rheumatoid Arthritis mass so takes longer.

  • Idiopathic disease

  • Immune-mediated destruction of joints

  • Rheumatoid factors (IgM and IgG) target blood cells and synovial membranes forming antigen-antibody complexes

  • Genetic predisposition

  • Possibly bacterial or viral infection (Epstein-Barr)

Rheumatoid arthritis59 l.jpg
Rheumatoid Arthritis mass so takes longer.

  • Chronic inflammation of synovial membrane

  • Cellular proliferation and damage to the microcirculation

  • Synovial membrane becomes irregular

  • Swelling, stiffness and pain

  • Cartilage and bone destruction

  • Ankylosis or fusing of joint

  • Ligaments and tendons also affected

Rheumatoid arthritis60 l.jpg
Rheumatoid Arthritis mass so takes longer.

  • Systemic effects:

    • Generalized weakness and malaise

    • Up to 35% develop granulomas called rheumatoid nodules

    • Systemic inflammation of blood vessels – rheumatoid vasculitis

    • Serous membranes may be affected

Rheumatoid arthritis61 l.jpg
Rheumatoid Arthritis mass so takes longer.

  • Evaluation :

    • Physical examination

    • X-ray

    • Serologic tests for rheumatoid factor and circulating antigen-antibody complexes

  • No cure

Rheumatoid arthritis62 l.jpg
Rheumatoid Arthritis mass so takes longer.

  • Therapy:

  • Relieve pain and swelling and retain as much joint function as possible

  • Resting the joint, or binding or splinting

  • Use of hot and cold packs

  • Diet high in calories and vitamins

  • Strengthening of associated muscles

Rheumatoid arthritis63 l.jpg
Rheumatoid Arthritis mass so takes longer.

  • Drug therapy:

    • Methotrexate

    • Antimalarial drugs and immunosuppression

  • Surgical

    • Synovectomy

    • Correction of deformities

    • Joint replacement