OSTEOPOROSIS�

Issah J. kiswagala

(M.B.B.S)

INTRODUCTION

• Osteoporosis (thinning bones), is a disease characterized by low bone mass and structural deterioration of bone tissue, leading to bone fragility.
• Bones are weak with the increases risk of fracture.

CALCIUM METABOLISM REGULATION�

• The plasma ionized calcium concentration is regulated by Parathyroid hormone (Parathyroid gland), Calcitonin (Thyroid gland) and Vitamin D.
• Calcitonin decreases plasma ionized Calcium (Bone deposition), Parathyroid increases ionized plasma Calcium (Bone resorption), Vitamin D (Increases Intestinal absoption of Calcium).

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High plasma Calcium level.

• Thyroid gland increases their secretion of calcitonin which stimulate uptake of plasma calcium by bones and get deposited.
• At the same time the parathyroid glands reduce their rate of producing parathyroid hormone which inhibit removal of calcium from the skeleton.
• Low parathyroid hormone have several other effects such as increase the loss of calcium in the urine and  inhibit the loss of phosphate ions via that route.

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• Parathyroid hormone  inhibit the formation of Vitamin D3 from the kidney which will inhibit intestines their ability to absorb calcium.

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Low plasma Calcium level

• Calcitonin secretion is inhibited and parathyroid hormone secretion is stimulated  resulting in calcium being removed from bone to rapidly correct the plasma calcium level.
• High parathyroid hormone levels will inhibit calcium loss via the urine while stimulating the excretion of phosphate ions via that route.
• They also stimulate
• the kidneys to manufacture Vitamin D3 which enhances the ability of the cells lining the gut to absorb calcium from the intestinal contents into the blood.

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• Estrogen increases calcium absorption in the bowel and reabsorption in the kidney. In men effects occur due to local aromatization of Testosterone to estrogen.

• TEASER
• Soda and Osteoporosis:
• Phosphoric acid, a major component in most sodas, Phosphorus itself is an important bone mineral. But if you're getting a disproportionate amount of phosphorus compared to the amount of calcium you're getting, that could lead to bone loss. (Balance between Calcium and Phosphate).--- according to lead study author Katherine Tucker, PhD.

AETIOLOGY/RISK FACTORS

1. Estrogen deficiency (post-menopausal state) and testosterone deficiency, Estrogen acts on multiple cells via estrogen receptor with a net result of increased bone mineral density. Therefore, the deficiency of estrogen increases bone resorption, caused by increased osteoclast (bone eating cells) numbers and reduced their apoptosis.
• Bone cells do not have receptors for testosterone, rather its effect on bone is indirect through the local aromatization to estrogen.

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• Vitamin D insufficiency which impairs intestinal absorption of calcium
• Insufficient calcium intake can leads to secondary hyperparathyroidism, which increases the rate of bone remodelling to maintain a normal serum calcium levels.

4. Smoking

Use of cigarettes is detrimental to bone health by multiple mechanisms:

• Tobacco compounds have a direct toxic effect of osteoblasts (Bone forming cells).
• Estrogen metabolism is altered, leading to earlier menopause.
• Medications
• Glucocorticoids (e.g. prednisone) are the most common cause of medication-induced Osteoporosis. They  adversely affect bone metabolism by multiple mechanisms:
• Stimulation of osteoclast differentiation
• Inhibition of osteoblast proliferation
• Decrease in intestinal calcium absorption
• Increase in  renal calcium reabsorption

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• Other immunosuppressants, such as cyclosporine, can also cause rapid bone loss through similar mechanisms to glucocorticoids.

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6. Illnesses 
• Certain gastrointestinal disease result in impaired absorption of bone minerals and vitamin D and therefore contribute to Osteoporosis e.g. malnutrition, malabsorption syndromes (celiac and crohn’s disease).
• Endocrine disorders can impair bone health through a variety of mechanisms (e.g. Cushing syndrome, hyperparathyroidism)
•  hypogonadal states there is decreased functional activity of the gonads and the positive effects of estrogen on bone health is reduced (e.g. Turner’s syndrome, anorexia nervosa).
• Thyroid hormone directly stimulates bone resorption.  Endogenous thyrotoxicosis accelerates bone turnover and is a significant risk factor for development of Osteoporosis

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CLINICAL PRESESNTATION

• Osteoporosis generally does not become clinically apparent until a fracture occurs. 

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1. VERTEBRAL FRACTURES

• Two thirds of vertebral fractures are painless.
• The episode of acute pain may follow a fall or minor trauma
• Pain is localized to a specific, identifiable, vertebral level in the midthoracic to lower thoracic or upper lumbar spine.
• The pain is described variably as sharp, nagging, or dull; movement may exacerbate pain; in some cases, pain radiates to the abdomen.
• Pain is often accompanied by paravertebral muscle spasms exacerbated by activity and decreased by lying supine.
• Patients often remain motionless in bed because of fear of exacerbating the pain.

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2. HIP FRACTURE 

• Pain in the groin, posterior buttock, anterior thigh, medial thigh, and/or medial knee during weight-bearing or attempted weight-bearing of the involved extremity
• Diminished hip range of motion (ROM), particularly internal rotation and flexion
• External rotation of the involved hip while in the resting position

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3. COLLES FRACTURES

• Pain on movement of the wrist
• Dinner fork (bayonet) deformity

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• Others Kyphosis or dowager hump or loss of height due to Progressive vertebral compression fractures. 

DIFFERENTIAL DIAGNOSES�

• Multiple Myeloma
• Paget Disease
• Osteomalacia
• Pathologic fractures secondary to bone metastases from cancer
• Pediatric osteogenesis imperfecta

INVESTIGATIONS

• Complete blood count: May reveal anemia
• Serum chemistry levels: levels of serum calcium, phosphate, and alkaline phosphatase are usually normal in persons with primary osteoporosis, although alkaline phosphatase levels may be elevated for several months after a fracture.
• Creatinine levels may decrease with increasing parathyroid hormone.
• Liver function tests: Increased levels AST, ALT, Bilirubin and alkaline phosphatase may indicate alcohol abuse.
• Hormonal tests, testosterone (total and/or free) and luteinizing hormone/follicle-stimulating hormone: Male hypogonadism and post menopausal are associated with osteoporosis
• Plain X ray may be indicated if a fracture is already suspected (Decreased bone density can be appreciated by decreased cortical thickness and loss of bony trabeculae in the early stages)

TREATMENT

• Calcium and vitamin D:
• Calcium supplementation of 1000 – 2000 mg/day is recommended, taken in doses of ≤ 600 mg to maximize absorption.
• Vitamin D should be supplemented in conjunction with calcium at a dose between 400 and 2000 IU/day.
• Estrogen controversy surrounds its use given potential increase in cardiovascular disease and breast cancer and therefore appropriate patient selection must be employed when starting hormone replacement therapy.
• Bisphosphonates: (Oral bisphosphonates are the most commonly prescribed medications and are effective in reducing the risk of further osteoporotic fracture)
• Bisphosphonates are analogues of pyrophosphates which are compounds naturally found in bone matrix and act by specifically impairing the action of osteoclasts and inducing apoptosis of osteoclasts.
• Alendronate, risendronate and ibandronate are approved for the prevention and treatment of osteoporosis.

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• Selective estrogen-receptor modulators (SERMs):
• act as either agonists or antagonists of estrogen receptors. In bones, agonistic activity on estrogen receptor leads to a reduction in bone resorption.
• Currently, two SERMs (tamoxifen and raloxifene) have been shown to be beneficial in the treatment of post-menopausal osteoporosis.
• Lifestyle
• Exercise can be effective in preventing bone loss and improving balance, coordination and strength, thereby reducing risk of falls. 
• 30 minutes of weight-bearing exercise should be undertaken daily by patients who are able to tolerate it.
• Smoking cessation and minimizing alcohol consumption are also beneficial.
• Reducing medications and minimizing dosages, especially glucocorticoids, should be considered.

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PROGNOSIS

• The prognosis for osteoporosis is good if bone loss is detected in the early phases and proper intervention is undertaken.
• Patients can increase bone mass density and decrease fracture risk with the appropriate anti-osteoporotic medication.

FOLLOW UP

• If being treated with estrogen replacement therapy, patient should have routine mammograms, pelvic exams, and Pap smears to monitor the possible medication side effects.
• If on non-hormonal treatment, have urine and kidney function tests and routine follow-up.

PREVENTION

• Building strong bones during childhood and adolescence can be the best defense against developing osteoporosis later. The average woman has acquired 98% of her skeletal mass by 30 years of age.
• Eat a balanced diet rich in calcium and vitamin D and high in fruits and vegetables.
• Engage in weight-bearing physical exercise.
• Adopt a healthy lifestyle with no smoking or excessive alcohol intake.
• Take medication to improve bone density when appropriate.
• And avoid other risk factors.

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COMPLICATIONS

• Fractures and deformities
• Osteoarthritis.
• Bone cancer
• Spinal compression fractures
• kyphosis or Dowager's hump
• Height loss (results from multiple compression fractures in the spine).