This presentation discusses osteoporosis and bone remodeling. It defines osteoporosis and describes the categories. It then summarizes the six step process of bone remodeling, including the roles of osteoclasts and osteoblasts in resorbing and rebuilding bone. Estrogen's positive effects on this process are noted. The document also outlines the pathophysiology, diagnosis, and pharmacological and non-pharmacological treatment options for osteoporosis.
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Know more such facts and useful information on prevention of Osteoporosis.
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2. Definition
Osteoporosis is a skeletal disorder characterized by comprised
bone strength predispose individual to an increased fracture
risk.
Categories of osteoporosis include:
(1) postmenopausal osteoporosis,
(2) agerelated osteoporosis, and
(3) secondary osteoporosis.
3.
4. BONE FORMATION
Bone remodeling is a dynamic process that occurs continuously
throughout life.
STEP 1: INTIATION OF BONE REMODELLING
The complete physiology of bone remodeling is not fully known but
appears to begin with signals from lining cells or osteocytes
(bonecommunication cells) that are triggered by stress, microfractures,
biofeedback systems, and potentially certain diseases and medications.
Many cytokines, growth factor and hormone influence each remodeling
step.
5.
6. STEP 2: DIFFERENTIATION AND ACTIVATION
OSTEOCLAST
A major stimulus for hematopoietic stem cell (monocyte–
macrophage lineage) differentiation to become mature
osteoclasts (bone resorbing cells) is the receptor activator of
nuclear factor kappa B ligand (RANKL), which is emitted from
the osteoblast (bone-forming cells) in step 2 and binds to its
receptor RANK on the surface of osteoclast precursors.
RANKL also stimulates mature osteoclast activation and bone
adherence via integrins to resorb bone.
7. STEP3: OSTEOCLASTIC BONE RESORPTION
Proteinases are secreted to resorb the protein matrix, and hydrogen
ions are secreted to dissolve the mineralized component (step 3).
STEP 4: REVERSAL-SWITCH FROM RESORPTION TO
FORMATION
After bone is resorbed and a cavity is created, additional cytokines
and growth factors some working through Wnt/ β -catenin pathways,
are released that first mature osteoblasts from mesenchymal stem
cells and then stimulate bone formation
Osteoclasts also produce ephrinB2 that adhe to ephB4 receptors
on osteoblasts and osteoblast precursors to stimulate osteoblast
differentiation and activity.
Mature osteoblasts produce osteoprotegerin (OPG) that binds to
RANKL, thereby stopping bone resorption.
8. STEP 5: OSTEOBLASTIC BONE FORMATION
Bone formation occurs over two phases.
First, osteoblasts fill the resorption cavity with osteoid, and then
mineralization occurs.
STEP6: QUIESCENCE-RESTING BONE
Once bone formation is complete, mature osteoblasts undergo
apoptosis or become lining cells or osteocytes.
Osteocytes produce sclerostin, which inhibits Wnt signaling and
bone formation.
Quiescence is the phase when bone is at rest until another
remodeling cycle is initiated at that site.
9. Estrogen has many positive effects on the bone remodeling
process, with most of its actions helping to maintain a normal bone
resorption rate.
Estrogen suppresses the proliferation and differentiation of
osteoclasts and increases osteoclast apoptosis.
Estrogen decreases the production of several cytokines that are
potent stimulators of osteoclasts, including interleukins 1 and 6, and
tumor necrosis factor- α .
Estrogen also decreases the production of RANKL and increases
the production of OPG, both of which reduce osteoclastogenesis
10. Pathophysiology
Bone loss occur when bone resorption exceed bone formation
Men & women began to loose a small amount of bone mass starting
in the third or fourth decade as a consequence of reduced bone
formation.
Estrogen deficiency during menopause increase proliferation,
differentiation and activation of few osteoclast prolongs survival of
mature osteoclast this increase bone resorption more than
formation.
Age related osteoporosis occurs mainly because of hormone,
calcium and vitamin D deficiencies lead into accelerated bone
turnover and reduced osteoblast formation.
11. cont….
Drug induced osteoporosis may result from systemic
corticosteroids (prednisone doses greater than 7.5 mg/day)
thyroid hormone replacement, some antiepilectic drugs
(phenytoin, phenobarbital).
12. Diagnosis
Physical examination findings: bone pain, postural changes (ie, kyphosis), and loss of
height (>1.5 in [3.8 cm]).
• Laboratory testing: complete blood count, creatinine, blood urea nitrogen, calcium,
phosphorus, alkaline phosphatase, albumin, thyroid-stimulating hormone, free
testosterone,25-hydroxyvitamin D, and 24-hour urine concentrations of calcium and
phosphorus
Measurement of central (hip and spine) BMD with dual-energy x-ray
absorptiometry (DXA) is the diagnostic standard. Measurement at peripheral
sites (forearm, heel,and phalanges) with ultrasound or DXA is used only for
screening and for determining need for further testing.
A T-score compares the patient’s measured BMD to the mean BMD of a healthy,
young (20- to 29-year-old), gender-matched, white reference population.
The T-score is the number of standard deviations from the mean of the reference
population.
13. Diagnosis of osteoporosis is based on low-trauma fracture or central hip
and/or spine DXA using WHO T-score thresholds.
Normal bone mass is T-score above -1, low bone mass (osteopenia) is
T-score between -1 and -2.4, and osteoporosis is T-score at or below-
2.5.
Osteopenia is a classification for bone denisty that is precursor to
osteoporosis.
Bone denisty is lower than normal but more than in osteoporosis.
Osteopenia may develop as some people have lower bone denisty than
normal, it may also develop due to other disease such as eating
disorder,digestive or metabolism problem as well as the treatment of disease
including certain medication, chemotherapy or radiation.
Osteoporosis occurs when a person has a very low bone density that
significantly increases his or her risk of fracture.
14. Pharmacotherapy
Non Pharmacologic therapy
Balanced diet with adequate calcium & vitamin d.
Caffeine intake should be limited.
Alcohol consumption should not exceed one drink per day for
women and two drinks per day for men
17. Pharmacologic therapy
ANTIRESORPTIVE THERAPY
CALCIUM
Calcium should be ingested in adequate amount to prevent
secondary hyperparathyroidism and bone destruction.
Calcium increases BMD fracture prevention is minimal
Calcium carbonate is the salt of choice.
18. DRUG CALCIUM
ADULT DOSAGE
PHARMACOKINETI
C
ADVERSE EFFECT
DRUG
Adult:(19-50yr)1000-2500mg,(51-70yr)men1000-2000mg
women1200-2000; >70yrs 1200-200mg.
Absorption predominatly active transport with some passive diffu
fractional absorption 10-60%
Constipation gas upset stomach rare kidney stones
Carbonate salts decreased absorption with proton pump inhibitor
19. VITAMIN D SUPPLEMENTATION
Vitamin D maximizes intestinal calcium absorption and has been shown to
increase BMD it may also reduce fractures.
DRUG ADULT DOSAGE PHARMACOKINETICS DRUG
INTERACTION
1,25(OH)2 0.25-0.5mcg orally - might induce hypercalcemia
VITAMIN D
D2 50,000 Units once weekly - cholestyramine ,colestipol
or once monthly. mineral oil decrease
vitamin d absorbtion .
D3 adult(19-70yr)600-4000* hepatic metaboliasm to25(oh) phenytoin barbiturates
rifampin
>70yr 800-4000* vitamin d & then renal metabolism increase vitamin d
metabolism .
*(unit) to active compound
20. BISPHOSPHONATES
Bisphosphonate bind to hydroxyapatite in bone and decrease
resorption by inhibiting osteoclast to adherence to bone surfaces.
Alendronate, risedronate ,oral ibandronate are FDA approved for
prevention and treatmentof post menopausal osteoporosis.
IV ibandronate & zoledronic acid indicated only for treatment of
postmenopausal women.
The most common adverse effect are nausea abdominal pain
dyspesia, esophageal, gastric, or duodenal irritation, perforation,
ulceration, or bleeding may occur when administration directions are
not followed or when bisphosphonates are prescribed for patients with
contraindications.
The most common adverse effects of IV bisphosphonates include
fever, flu-like symptoms, and local injection-site reactions
21. DRUG ADULT DOSAGE PHARMACOKINETICS ADVERSE EFFECT DRUG
INTERACTION
Alendronate 5mg daily,35 mg poorly absorbed nausea, heartburn do not
coadminister
(fosamax) 35mg weekly with zero food or ulceration with any other
medicine
beverage
Risedronate 5mg daily,35mg
(actonel) weekly,150mg
Monthly
Ibandronate 2.5mg daily
(boniva) 150mg monthly
22. INTRAVENOUS BISPHOSPHONATES
DRUG ADULT DOSAGE PHARMACOKINETICS ADVERSE EFFECT DRUG
INTERACTION
IBANDRONATE 5mg early muscle
pain,redness
(BONIVA) ------ ----- or swelling at
ZOLEDRONIC ACID injection site
(RECLAST) blackbox
warning
for rare
osteonecrosis
of the jaw
23. CALCITONIN
Calcitonin is an endogenous hormone released from the thyroid gland when
serum calcium is elevated. Salmon calcitonin is used clinically because it is more
potent.
Calcitonin may provide some pain relief in patients with acute vertebral fractures.
Calcitonin is indicated for osteoporosis treatment for women at least 5 years post
menopause. It is reserved as a last-line treatment
Drug adult dosage pharmacokinetics adverse effect drug
interaction
Calcitonin 200 units intranasal renal elimination rhinitis,epistaxis
none
(MIACALCIN) daily 3% nasal availability
24. ESTROGEN THERAPY
Estrogens are FDA-indicated for prevention of osteoporosis in women at
significant risk and for whom other osteoporosis medications cannot be
used.
Hormone therapy (estrogen with or without a progestogen) significantly
decreases fracture risk.
Oral and transdermal estrogens at equivalent doses and continuous or cyclic
regimens have similar BMD effects.
When therapy is discontinued, bone loss accelerates and fracture protection
is lost.
25. TESTOSTERONE
Testosterone replacement is not FDA approved for the prevention or
treatment of osteoporosis.
1.25 or 2.5 mg daily or testosterone implants 50 mg every 3 months had
increased BMD.
Testosterone may increase BMD in men with low testosterone
concentrations but has no effect if testosterone concentrations are normal.
26. DRUG ADULT DOSAGE
TRANSDERMAL PATCHES 5mg patch applied to arm back or thigh
every evening.
(TESTODERM TTS)
(ANDRDERM TESTIM)
GEL(ANDROGEL1%) 5g gel applied to shoulder,upper arm or
abdomen
(TESTIM1%) every morning
BUCCAL SYSTEM(STRIANT30mg) place one system in gum area twice a
day
INJECTION
METHYLTESTOSTERONE 1.25-2.5mg with esterified estrogen
Cypionate 100-200mg im every 2-3 weeks.
27. MIXED ESTROGEN
AGONIST/ANTAGONIST
Raloxifene is an Estrogen agonist on bone but an antagonist on the breast and uterus.
Approved for prevention & treatment of postmenopausal osteoporosis.
Raloxifene decreases vertebral fractures and increases spine and hip BMD, but to a lesser
extent than bisphosphonates.
After discontinuation, the beneficial effect is lost, and bone loss returns to age- or disease-
related rates.
Raloxifene is well tolerated overall. Hot flushes, leg cramps, and muscle spasms are common.
Raloxifene is contraindicated in women with an active or past history of venous thromboembolic
disease.
Drug brand name: evista
Dose:60mg daily
Pharmacokinetics: hepatic metabolism
28. DENOSUMAB
Denosumab (Prolia) is a RANK ligand inhibitor that inhibits osteoclast formation
and increases osteoclast apoptosis. It is indicated for treatment of osteoporosis in women
and men at high risk for fracture
Denosumab is contraindicated in patients with hypocalcemia until the condition is corrected.
DRUG ADULT DOSAGE PHARMACOKINETICS ADVERSE
EFFECT
Denosumab 60mcg subcutaneously Tmax~10 days
flatulence,dermitis,
(prolia) every 6 months T1/2~25.4days eczema,rash
rare: hypocalcemia
serious infection
29. THIAZIDE DIURETICS
Thiazide diuretics increase urinary calcium reabsorption.
Prescribing thiazide diuretics solely for osteoporosis is not recommended but is a
reasonable choice for patients with osteoporosis who require a diuretic and for patients on
glucocorticoids with a 24-hour urinary calcium excretion >300 mg.
30. ANABOLIC THERAPY
•Teriparatide is a recombinant product representing the first 34 amino acids in human
parathyroid hormone. Teriparatide increases bone formation, the bone remodeling rate, and
osteoblast number and activity. Both bone mass and architecture are improved.
Transient hypercalcemia rarely occurs. Teriparatide is contraindicated in patients at
increased risk for osteosarcoma.
Drug adult dosage pharmacokinetics adverse effect drug
interaction
Teriparatide 20mcg 95% bioavailability pain at injection site
(forteo) subcutaneously daily T1/2~60 min nausea,headache , none
up for 2 years hepatic metabolism dizziness,increase in uric
Tmax~30 min acid
31. NEWER DRUGS
ANTIRESORPTIVE THERAPIES
SERMs
Newer drugs that are in various stages of drug development include
bazedoxifene, lasofoxifene &arzoxifene.
These drugs have shown to be effective in preventing bone loss, preserving
bone strength and reducing total cholesterol levels without evidence of
endometrial stimulation and fewer incidences of hot flushes
Bazedoxifene & lasofoxifene have been approved in europe but not by US
FDA
32. OSTEOPROTEGERIN
It binds to RANKL and prevents its binding to RANK and hence the
activation of osteoclasts, thus acting as a natual antibody to the rankl.
Low bone turnover induced by OPG overexpression lead to increase
bonemass (preclinical studies)
C-src kinase inhibitors
Non receptor tyrosine kinase
Plays an important role in osteoclastic bone resorption
33. Cathepsin k inhibitors
Cathepsin k is a cysteine proteases that cleaves collagen1& help in bone
resorption
Drugs include odanacatib & balicatib that increases spine & hip BMD
CHLORIDE CHANNEL INHIBITORS
Passive movement of chloride through chloride channel(CLCN7) located in
the cell membrane of the osteoclast is required for secretion of acid from
osteoclast
ClCN7 inhibitor decrease osteoclast acidification and inhibit the formation
resorption pits.
35. ANABOLIC THERAPIES
CALCIUM SENSING RECEPTOR ANTAGONISM
Orally administered agents that stimulates endogenous PTH release & have
bone forming action
JTT-305 &SB-423557 are two calcilytics that shown increase in bone
formation & prevent bone loss (rats).
STATINS
Enhancers of the bone morphogenetic protein -2 gene expression & bone
formation (increase of osteoblastic number & promotion of osteoblastic
differentiation leading onto bone formation.
36. CANNABINOID AGONIST
Endocannabinoid & their receptors have been seen to be
involved in the regulation of osteoblast differentiation & bone
formation.
CP55940 & HU308
ACTIVIN INHIBITOR
ACTIVIN is a negative regulator of bone mass that stimulates
bone resorption & inhibit bone formation
37. MATRIX EXTRACELLULAR
PHOSPHOGLYCOPROTEIN(MEPE) FRAGMENTS
Highly expressed in differentiated osteoblasts and osteocytes and acts as
an endogenous inhibitor of bone formation
Deletion of MEPE gene in a mice leads to an increase in the number and
activity of osteoblasts leading to incresed bone mass
MEPE 242-264 a fragment of MEPE stimulayte new bione formation &
fracture healing in preclinical studies.