SEMINAR ON PHARMACOTHERAPY OF OSTEOPOROSIS
SEMINAR ON PHARMACOTHERAPY OF OSTEOPOROSISFACILITATED BY:DR.RAJU KONERI SIRHOD of Pharmacology departmentSUBMITTED BY:Dipankar acharjeeM.Pharmacy 1st yearDepartment pharmacology
Osteoporosis is defined as a skeletal disorder characterized by compromised bone strength predisposing a person to an increased risk of fracture
The development of osteoporosis is multifactorial, beginning with genetics and unhealthy bone lifestyles, along with other skeletal factors, which lead to compromised bone strength, and nonskeletal factors
PATHOPHISIOLOGYBone is comprised of three types of cell.Osteoblasts.Osteocytes. osteoclasts.
Osteoblast:-These are mononucleate bone-forming cells. Osteoblasts also manufacturehormones.Osteocytes:- These are mostly inactive osteoblasts.Osteoclast:-Theseare the cells responsible forbone resorption, thus they break down bone. New bone is then formed by the osteoblasts. Bone is constantlyremodelled by the resorption of osteoclasts and created by osteoblasts.Bone remodelling
Bone remodelling is a dynamic process that occurs continuously throughout life. The purpose of remodelling is to regulatecalcium homeostasis, repairmicro-damaged bonesfrom everyday stress.The action of osteoblasts and osteoclasts are controlled by a number of chemicalenzymesthat either promote or inhibit the activity of the bone remodeling cells, controlling the rate at which bone is made, destroyed, or changed in shape.
In osteoporosis,, bone mass (the amount of bone tissue) is reduced because its deposition does not keep pace with resorption. Peak bone mass occurs around 35 years and then gradually declines in both sexes. Lowered oestrogen levels after the menopause are associated with a period of accelerated bone loss in women. Thereafter bone density in women is less than in men for any given age. Bone is progressively weakened with cancellous bone affected first by thinning and loss of trabeculae. In the postmenopausal period an imbalance of hormones probably causes bone weakening.Filling the interior of the bone is thecancellous bonealso known as trabecular or spongy bone tissue.It is an open cellporousnetwork.5POSTMENOPAUSAL OSTEOPOROSISThe accelerated bone loss during perimenopause and postmenopause results from enhanced resorption mainly as a result of the loss in ovarian hormone production, specifically estrogen. Estrogen deficiency increases proliferation, differentiation, and activation of new osteoclasts and prolongs survival of mature osteoclasts. The number of remodeling sites increases and resorption pits are deeper and inadequately filled by normal osteoblastic function.Men are at a lower risk for developing osteoporosis and osteoporotic fractures because of larger bone size, greater peak bone mass, and fewer fallsThe etiology of male osteoporosis tends to be multifactorial with secondary causes and aging being the most common contributing factorsMALE OSTEOPOROSISSECONDARY CAUSES OF OSTEOPOROSIS
CausesThe major factors influencing bone losses are hormonal status, exercise, aging, nutrition, lifestyle, disease states, medications, and some genetic influences. Non hormonal risk factors are similar between women and men.
LOW BONE DENSITY: Bone loss occurs when bone resorption exceeds bone formation. Bone resorption sites greatly exceed the rate and ability of osteoblasts to form new bone. During peri-menopause and for up to 5 to 7 years after menopause, women can experience an accelerated rate of bone loss because of the drop in circulating estrogen and an increase in bone resorption
Osteopenia (low bone mass)10IMPAIRED BONE QUALITYThe strength of bone is highly impacted by the quality of the bones material properties and its structure. . Bone quality assessment is important because changes in bone quality effect bone strength much more than bone mass changesFALLSRisk of falling increases with advanced age predominantly as a result of balance, gait, and mobility problems, poor vision, reduced muscle strength, impaired cognition, multiple medical conditions
PREVENTION AND TREATMENTOsteoporosis prevention and treatment begins with a bone-healthy lifestyle and uses non prescription and prescription medications as needed.
The primary goal of osteoporosis management should be prevention.
Once osteopenia or osteoporosis develops, the objective is to stabilize or improve bone mass and strength and prevent fractures.
NONPHARMACOLOGIC THERAPYDiet:- Overall, a diet well balanced in nutrients and minerals is important for bone health. In addition, limiting intakes of caffeine, alcohol, sodium, cola, and other carbonated beverages. Excessive caffeine consumption is associated with increased calcium excretion, increased rates of bone loss, and a modest increased risk for fracture.
Calcium:- Data clearly indicate that adequate calcium intake is necessary for the development of bone mass during growth and for its maintenance throughout life.
Vitamin D:- The three main sources of vitamin D are sunlight, diet, and supplements. Because few foods are naturally high or fortified with vitamin D .(at least 800 to 2,000 units of vitamin D daily are needed)Other Nutrients and Minerals:-
Protein :-Dietary protein represents a key nutrient for bone health , evidence suggests that low protein intakes increase osteoporosis risk and that higher protein intakes are protective against bone.
Dietary SoyIsoflavone phytoestrogens are plant-derived compounds that possess weak estrogenic agonist and antagonist effects. The most common source for isoflavone is dietary soy products. Genistein is the most abundant and biologically active isoflavone in soybeans. SmokingSmoking cessation can help to optimize peak bone mass, minimize bone loss, and ultimately reduce fracture risk
ExercisePhysical activity or exercise is an important nonpharmacologic approach to preventing osteoporotic fractures. Exercise can decrease the risk of falls and fractures by improving muscle strength, coordination, balance, and mobility.
Fall PreventionBecause of the link between falls and fractures, homes should be made safe and potentially harmful medications eliminated.
Non-pharmacologic interventions alone frequently are insufficient to prevent or treat osteoporosis, drug therapy is often necessary.
AntiresorptiveAntiresorptive therapies include calcium, vitamin D, bisphosphonates, estrogen agonists/antagonists and calcitonin.
Calcium imbalance can result from inadequate dietary intake, decreased fractional calcium absorption, or enhanced calcium excretion. Adequate calcium intake is considered the minimal standard for osteoporosis prevention and treatment and should be combined with vitamin D and osteoporosis medications when needed.Adverse Events/Precautions:- Calciums most common adverse reaction constipation.
Vitamin D Supplementation
Vitamin D intake is critical for the prevention and treatment of osteoporosis because it maximizes intestinal calcium absorption.Seniors and patients being treated for osteoporosis should take at minimum 800 units of vitamin D through food and supplementation.
20BisphosphonateBisphosphonates mimic pyrophosphate, an endogenous bone reabsorption inhibitor. Bisphosphonates consistently provide the greatest fracture risk reductions and BMD increasesAdverse Events/Precautions;-Bisphosphonate GI adverse effects are minimal if the medication is taken correctly. Intravenous bisphosphonates include fever, flu-like symptoms.Each oral dose should be taken with at least 6 ounces of plain tap water at least 30 minutes before consuming any food.Mixed Estrogen Agonists/AntagonistsRaloxifene, a second generation mixed estrogen agonist/antagonist (EAA) approved for prevention and treatment of postmenopausal osteoporosis, is an estrogen agonist on bone. Raloxifene decreases vertebral fractures and increases spine and hip BMD
CalcitoninCalcitonin is FDA indicated for osteoporosis treatment for women who are at least 5 years past menopause.
Estrogen TherapyAlthough estrogens are FDA indicated for prevention of osteoporosis, they should only be used short-term in women who need estrogen therapy for the management of menopausal symptoms such as hot flushes.
Thiazide DiureticsIt increase urinary calcium reabsorption. Observational studies suggest that patients who receive thiazide diuretics have a greater bone mass, lower rates of bone loss, and fewer fractures
REFERENCESDipiro J.T. et al., Pharmacotherapy. A Pathophysiologic Approach. 7th ed. Pg. no. 1483-1504Waugh A, Grant A., Ross and Wilson Anatomy and Physiology in Health and Illness. 9th ed. Pg. no. 494THANK YOU