Path Bone 1 Ex 2

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Osteoporosis characterized by

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diffuse skeletal lesions due to a decreased mass of normally mineralized bone
There are both primary and secondary causes of osteoporosis

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The most common forms of the primary disorder are

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senile and post-menopausal osteoporosis

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Senile osteoporosis is a low turnover disorder, where bone is

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populated by poorly functional osteoblasts and osteoclasts

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menopausal osteoporosis, a high turnover situation exists meaning

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Normal bone formation with increased osteoclast activity
Decreased estrogen leads to increase in the secretion of certain cytokines (IL-1!!, IL-6 and M-CSF) from stromal cells; this action increases recruiting and activation of osteoclasts

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main difference in bone in most forms of osteoporosis and normal bone is

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increase in the amount of resorption. Bone formation levels are essentially normal

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Primary osteoporosis predisposing factors are

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genetic basis
adequate Ca2+ and vit D

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to prevent and treat osteoporosis in post-menopausal women

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Bisphosphonate therapy. Stronger forms are widely used in the management of advanced cancers that have metastasized to the bone

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bisphosphonates cause

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• Interfere with osteoclast cytoskeleton
• Stimulate apoptosis of osteoclasts
• Inhibit proton pump of osteoclasts

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How do bisphosponates act on osteoblasts?

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• Act on osteoblasts to inhibit stimulator of osteoclast recruitment
• Act on osteoblast to stimulate inhibitor of osteoclast recruitment
• Act on osteoblasts to inhibit osteoclast activity

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Secondary osteoporosis can develop with:

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Corticosteroid excess and alcohol inhibit osteoblastic activity. Hyperthyroidism and PTH lead to increased osteoclastic activity.

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Although Hormone Replacement Therapy was used to tx osteoporosis, it was shown that

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Slight increases in risk of heart attacks, strokes, and blood clots
Risk of invasive breast cancer increased by 25%

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Osteomalacia refers to

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the accumulation of unmineralized bone matrix resulting from a diminished rate of mineralization

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Rickets refers to

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accumulation of unmineralized bone matrix resulting from a diminished rate of mineralization
in a young person in whom the epiphysis are not yet closed

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Rickets may result due to

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dietary deficiency of vitamin D, defective bone mineralization or a variety of congenital or acquired defects in either vitamin D or phosphate metabolism

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the most common cause of osteomalacia in the United States

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Intestinal malabsorption (• Crohn’s disease
• Celiac disease
• Cholestatic liver disease
• Biliary obstruction
• Chronic pancreatitis
)

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Primary hyperparathyroidism is

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a metabolic disease leading to increased bone resorption do to excess PTH

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osteitis fibrosa cystica, The classic pathologic change in Primary hyperparathyroidism refers to

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the replacement of marrow by fibrous tissue, numerous microfractures and hemosiderin-laden macrophages. This is accompanied eventually by cystic degeneration and gives the classic gross appearance of a brown tumor.

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Paget disease is a chronic condition of bone characterized by

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1) initial osteoclastic lytic activity due to defective remodeling
2)disorganized and hyperplastic bone formation (osteoblastic phase),
3) burnt-out quiescent osteosclerotic stage

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Paget disease occurs in people

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older than 55 and Men are affected slightly more often than females The highest incidence is in England, Australia and the Western European plain

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Paget disease affects

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involves lumbosacral spine, pelvis and skull; very rare in ribs

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Complications of Paget’s Disease

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Pain
Fractures
Degenerative arthritis
Bone tumors (osteosarcoma, fibrosarcoma, chondrosarcoma and GCT)
High-output cardiac failure

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Osteogenesis imperfecta refers to a group of autosomal dominant heritable disorders of connective tissue, caused by

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mutations in the gene for type I collagen

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Most types of Osteogenesis imperfecta (except type IV) are also characterized by

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blue sclera, a finding attributed to the underlying choroids being visualized through the thin sclera.

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Osteopetrosis, also known as marble bone disease or Albers-Schönerg’s disease, is an inherited lysosomal defect resulting in

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in defective osteoclastic activity Bones are extremely dense, weighing 2-3 times normal. The most common, autosomal recessive form is a severe, sometimes lethal disease affecting infants and children

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Death due to Osteopetrosis is secondary to

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anemia, cranial nerve entrapment, hydrocephalus and infection

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Osteopetrosis treated with

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bone marrow transplantation

interferon gamma (IFN-γ).

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Bone Fractures involve breaks in continuity with

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bone, periosteum, blood vessels and sometimes muscles

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The speed of return to a normal state following fracture depends upon a number of factors including:

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age and nutritional status of the patient, severity of fracture, vascularity of the area and type of treatment applied

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Following a fracture the following takes place

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2-3 days-hematoma begins with in the ingrowth of capillaries (neovascularization
7 day-Intramembranous bone growth

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Formation of primary callus at fracture site

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Pluoripotent mesenchymal cells->osteoblasts->cartilage reabsorbed by endochondral ossification->primary callus->lamellar bone

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Osteomyelitis is a Bacterial infection of bone caused by

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Coagulase-positive Staph (70-90% of cases)
Klebsiella
Pseudomonas (“tennis shoe” osteo)
Neisseria

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Salmonella osteomyelitis is common in

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sickle cell disease.

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Hematogenous osteomyelitis occurs most often in

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patients under 20 years and involves the bones of the lower extremity in about 75% of cases.

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Chronic osteomyelitis is often incurable by antibiotics and often requires

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surgical debridment.

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Tuberculous osteomyelitis is a hematogenous infection seen in

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young adults. The bones most often infected are the vertebrae and bones of the hip, knee, ankle, elbow and wrist
Metaphyseal infection common in children
epiphyseal infection is more common in adults

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Fibrous Dysplasia is Non-neoplastic condition that can manifest as

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Monostotic variety

Polyostotic variety

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Fibrous Dysplasia Monostotic variety

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Older children and young adults
Accounts for 70% of all cases
M = F
May involve rib, femur, tibia, mandible or humerus
Does NOT develop into polyostotic form

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Polyostotic variety

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Multiple bones, usually with unilateral distribution
May (3%) or may not (27%) be associated with endocrine dysfunction
If associated with endocrine dysfunction, precocious puberty in females and areas of cutaneous hyperpigmentation (McCune-Albright syndrome); mutation of c-fos oncogene

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Fibrous Dysplasia Microscopically

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show curved, misshapen bone trabeculae interspersed with fibrous tissue of various cellularity. Coarse, woven bone NEVER becomes transformed to lamellar bone. Rows of osteoblasts are not present around the trabeculae.

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Treatment of fibrous dysplasia consists of

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curettage and repair of fractures.

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Most common form of joint disease

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Osteoarthritis-Elderly or status post trauma

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The cartilage degradation in osteoarthritis is believed to be mediated by

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cytokines, in particular IL-1 and TNF-α.

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Rheumatoid Arthritis involves

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Chronic systemic disease of unknown etiology
Joints of hands and feet nearly always involved; may involve elbows, knees, ankles, hips, spine and TMJ

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Rheumatoid Arthritis strongly associated with

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HLA-DR4 and several non-MHC genes

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Rheumatoid Factor

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Positive in 70-80% of patients with classic RA
Autoantibodies of IgM, IgG or IgA class that react with Fc region of IgG
Not specific for RA
Circulating complexes bind complement

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Rheumatoid Arthritis Synovial hyperplasia driven

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by IL-1

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ankylosing spondylitis and Reiter syndrome. Both of these disorders have a predilection for

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young men and are associated with HLA-B27

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Ankylosing spondylitis involves

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the vertebral column and sacro-iliac joints.

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. Reiter syndrome classically occurs following an

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episode of venereal disease and is characterized by the triad of urethritis, conjunctivitis and seronegative polyarthritis