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Transcript of Osteoporosis , causes , last update
OSTEOPOROSIS
INTRODUCTION
Osteoporosis, a chronic, progressive disease of
multifactorial etiology . It has been most frequently
recognized in elderly white women, although it does
occur in both sexes, all races, Osteoporosis is a
systemic skeletal disease characterized by low
bone mass and microarchitectural deterioration of
bone tissue, with a consequent increase in bone
fragility. The disease often does not become
clinically apparent until a fracture occure.
Normal bone formation and remodeling
Bone is continually remodeled throughout our lives in response to microtrauma. .bone resorption is always followed by bone formation, a phenomenon referred to as coupling.
Bone strength is determined by collagenous proteins and mineralized osteoid (compressive strength). The greater the concentration of calcium, the greater the compressive strength. In adults, approximately 25% of trabecular bone is resorbed and replaced each year, compared with only 3% of cortical bone.
Osteoclasts are responsible for bone resorption, whereas osteoblasts are responsible for bone formation . The 2 types of cells are dependent on each other for production and linked in the process of bone remodeling. In osteoporosis, the coupling mechanism between osteoclasts and osteoblasts is thought to be unable to keep up with the constant microtrauma to trabecular bone. Osteoclasts require weeks to resorb bone, whereas osteoblasts need months to produce new bone. Therefore, any process that increases the rate of bone remodeling results in net bone loss over time.
ESTROGEN DEFICIENCY
Estrogen deficiency not only accelerates bone loss
in postmenopausal women but also plays a role in
bone loss in men. Estrogen deficiency can lead to
excessive bone resorption accompanied by
inadequate bone formation. in the absence of
estrogen, T cells promote osteoclast recruitment,
differentiation, and prolonged survival .T cells also
inhibit osteoblast differentiation and activity and
cause premature apoptosis of osteoblasts . Finally,
estrogen deficiency sensitizes bone to the effects of
parathyroid hormone (PTH).
AGING
In contrast to postmenopausal bone loss, which is
associated with excessive osteoclast activity, the
bone loss that accompanies aging is associated
with a progressive decline in the supply of
osteoblasts in proportion to the demand.
CALCIUM DEFICIENCY
Calcium, vitamin D, and PTH help maintain bone
homeostasis. Insufficient dietary calcium or
impaired intestinal absorption of calcium due to
aging or disease can lead to
secondary hyperparathyroidism. PTH is secreted in
response to low serum calcium levels. It increases
calcium resorption from bone, decreases renal
calcium excretion, and increases renal production
of 1,25-dihydroxyvitamin D (1,25[OH]2 D)—an
active hormonal form of vitamin D that optimizes
calcium and phosphorus absorption, inhibits PTH
synthesis, and plays a minor role in bone
resorption.
ADDITIONAL FACTORS AND CONDITIONS
Endocrinologic conditions or medications that lead
to bone loss (eg, glucocorticoids) can cause
osteoporosis. Corticosteroids inhibit osteoblast
function and enhance osteoblast apoptosis .
Other factors implicated in the pathogenesis of
osteoporosis include polymorphisms in the vitamin
D receptor; alterations in insulin-like growth factor-
1, bone morphogenic protein, prostaglandin E2,
nitrous oxide, and leukotrienes; collagen
abnormalities
RISK FACTORS
1. Advanced age (≥50 years)
2. Female sex
3. White or Asian ethnicity
4. Genetic factors, such as a family history of osteoporosis
5. Thin build or small stature (eg, body weight less than 127 lb)
6. Amenorrhea
7. Late menarche
8. Early menopause
9. Postmenopausal state
10. Physical inactivity or immobilization[38]
11. Use of drugs: anticonvulsants, systemic steroids, thyroid
supplements, heparin, chemotherapeutic agents, insulin
12. Alcohol and tobacco use
13. Androgen[39] or estrogen deficiency
14. Calcium deficiency
PREVENTION OF OSTEOPOROSIS
Diet — An optimal diet for preventing or treating osteoporosis includes consuming an adequate number of protein and calories as well as optimal amounts of calcium and vitamin D
Exercise — Exercise may decrease fracture risk by improving bone mass in premenopausal women and helping to maintain bone density for women after menopause.
Smoking — Stopping smoking is strongly recommended for bone health because smoking cigarettes is known to speed bone loss.
Falls — Falling significantly increases the risk of osteoporotic fractures in older adults. Taking measures to prevent falls can decrease the risk of fractures.
OSTEOPOROSIS TREATMENT MAY ALSO BENEFIT
BREAST CANCER PATIENTS
Date:
October 2, 2014
Source:
McGill University Health Centre
Summary:
According to a study, findings show that medication used to treat bone deterioration in post-menopausal women may also slow skeletal metastasis caused from breast cancer. This study is among the first to link bisphosphonate use with improved survival in women with breast cancer.
TEETH PROTEIN PROMISES BONE REGENERATION
Date:
July 2, 2014
Source:
Queen Mary, University of London
Summary:
Patients suffering from osteoporosis or bone fractures might benefit from a new discovery of a protein that plays an important role in bone regeneration made by bioengineers. Normally found in the formation of enamel, which is an important component of teeth, the scientists discovered that a partial segment of the protein statherin can be used to signal bone growth.
OBESITY CAN AMPLIFY BONE, MUSCLE LOSS
Date:
April 16, 2014
Source:
Florida State University
Summary:
A new syndrome called “osteosarcopenic obesity” that links the deterioration of bone density and muscle mass with obesity has been identified by researchers. The syndrome explains how many obese individuals experience a triad of problems that place them at a higher risk for falling and breaking bones. Researchers note that the work stands to remind people to consider the damage that can be done to all parts of the body if they are overweight.
RESOURCES
1- www.sciencedaily.com
2- www.uptodate.com
3- emedicine.medscape.com
4- en.wikipedia.org