1

Review of Musculoskeletal System

Chapter 36

2

Skeletal System• Function:

– Protection– Hematopoiesis– Mineral homeostasis

• Calcium• Phosphorus• Carbonate• Magnesium

3

Structure

• Bone is a connective tissue:– Matrix

• Collagen fibers for flexibility and tensile strength

• Calcium for rigidity

• Hydroxyapatite Ca5(PO4)3OH

4

• 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

5

6

7

Types of Bone

• Dense or Compact (85%) – Osteon (Haversian System)– Central (Haversian) canal– Lamellae– Lacunae with osteocytes– Canaliculi

• Spongy (cancellous) bone (15%)– trabeculae

8

9

10

11

Periosteum

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

• Inner layer– Osteoblasts– Anchored to bone by collagen fibers that

penetrate into bone

12

Bone Formation

• Endochondral ossification– Inside hyaline cartilage– Most bones

• Intramembranous ossification– Forms directly inside membranes– Bones of skull

13

14

Growth

• Lengthening of bones at epiphyseal plate– Grows from cartilage

• Forms epiphyseal line when done growing

• Undergoing constant remodeling– Adaptation to stress– Healing

15

16

Skeleton• 206 bones

• Axial skeleton– Skull and hyoid– Vertebral column– Ribs and sternum

• Appendicular skeleton– Shoulder girdle– Pelvic girdle

17

Classification• Long bones:

– Diaphysis

– Epiphysis

– Metaphysis

– Medullary cavity

– Endosteum

18

19

Classification cont.• Short bones

• Flat bones

• Irregular bones

• Sesamoid bones

• Wormian bones

20

21

22

Joints

• Degree of movement

– Synarthrosis – immovable joint

– Amphiarthrosis – slightly movable joint

– Diarthrosis – freely movable joint

23

• 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

24

25

• Synovial fluid

– Plasma filtrate

– Synovial cells and leukocytes phagocytize debris and microbes

• Articular cartilage

– Reduce friction

– Distribute force

26

27

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

28

• 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

29

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.

30

• 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

31

32

• 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.

33

• 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)

34

35

36

37

Risk factors• Family history

• White race

• Increased age

• Female sex

• Small stature

• Fair or pale skin

• Thin build

• Early menopause (natural or surgical)

• Late menarche

38

Risk factors cont.• 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.

39

• Often progresses silently for decades until fracture occurs

• 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

40

Clinical manifestations• 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

41

Treatment• 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

42

Prevention• 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

43

Rickets and Osteomalacia• Inadequate mineral deposition in

essentially normal organic matrix

• Softened bone:– Subject to malformation and distortion –pain

44

Rickets • 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

45

Osteomalacia• 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.

46

Joint Disorders• 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.

47

Osteoarthritis• 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

48

Osteoarthritis• 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

49

Osteoarthritis• 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

50

Osteoarthritis• 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

51

Osteoarthritis• 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

52

OsteoarthritisPrimary signs and symptoms of joint disease

are:

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

53

Osteoarthritis• 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

54

Osteoarthritis• 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

55

Rheumatoid Arthritis

• 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)

56

Rheumatoid Arthritis• 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

57

Rheumatoid Arthritis• 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

58

Rheumatoid Arthritis

• 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)

59

Rheumatoid Arthritis

• 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

60

Rheumatoid Arthritis

• 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

61

Rheumatoid Arthritis

• Evaluation :– Physical examination– X-ray– Serologic tests for rheumatoid factor and

circulating antigen-antibody complexes

• No cure

62

Rheumatoid Arthritis• 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

63

Rheumatoid Arthritis• Drug therapy:

– Methotrexate– Antimalarial drugs and immunosuppression

• Surgical– Synovectomy– Correction of deformities– Joint replacement