Pathophysiology of osteoporosis:
Low bone mass & micro architectural deterioration of bone tissue leading to increased fragility and a consequent increase in the risk of fractures even with little or no trauma.
Bone mass at the time of menopause and rate of bone loss following it, influence subsequent risk of fractures.
Peak bone mass is influenced by heredity and endocrine factors. After 30yrs in most of people slow decrease in bone mass density occurs approximately 0.7% per year.
This decrease accelerates after menopause and upto 5% of trabicular bone and 1.5% of total bone mass decrease occur per year. Trabicular bone resorption and formation occur 4 to 8 times as fast as cortical bone.
In the first 20 yrs following menopause 50% reduction in trabicular bone and 30% reduction in cortical bone occurs.
In absence of estrogen, osteoclastic activity increases leading to increased bone resorption by classic pathway involving genomic transcription by hormone receptors and a nongenomic pathway inhibits apoptosis.
Estrogen increases the availability of vitamin D which increase the absorption of calcium.
Estrogen also modulates the production of bone resorbing cytokines such as interleukin 1&6, bone stimulating factors as insulin like growth factors 1&2, colony stimulating factors, osteoprotegerin, tranforming growth factor-beta.
Estrogen is important hormone both in males & females.
Men with mutation in estrogen receptor alpha have aromatase deficiency grow slowly and have markedly reduced bone densities. Bone mass adjusted for body size is greater in black women than whites.
But they are subject to similar risk factors as thinness, alcohol consumption etc.
Around 75% of bone loss that occurs in women during the first 15yrs after menopause is due to estrogen deficiency rather than to aging it self.
Risk of fracture depends on two factors, the bone mass achieved at maturity and the subsequent bone loss.
The bone density, which is the threshold for vertebral fracture is only slightly lower than the lower limit of normal for premenopausal women.
Changes of bone remodeling
Pathophysiology
Signs and symptoms
Risk factors and investigations
Investigations
Diagnostic tests and biochemical markers
Hormonal treatment
Estrogen modulators, calcium
Vitamin D
Bisphosphonates
Calcitonin, Fluoride, Tibolone
Prevention
Low bone mass & micro architectural deterioration of bone tissue leading to increased fragility and a consequent increase in the risk of fractures even with little or no trauma.
Bone mass at the time of menopause and rate of bone loss following it, influence subsequent risk of fractures.
Peak bone mass is influenced by heredity and endocrine factors. After 30yrs in most of people slow decrease in bone mass density occurs approximately 0.7% per year.
This decrease accelerates after menopause and upto 5% of trabicular bone and 1.5% of total bone mass decrease occur per year. Trabicular bone resorption and formation occur 4 to 8 times as fast as cortical bone.
In the first 20 yrs following menopause 50% reduction in trabicular bone and 30% reduction in cortical bone occurs.
In absence of estrogen, osteoclastic activity increases leading to increased bone resorption by classic pathway involving genomic transcription by hormone receptors and a nongenomic pathway inhibits apoptosis.
Estrogen increases the availability of vitamin D which increase the absorption of calcium.
Estrogen also modulates the production of bone resorbing cytokines such as interleukin 1&6, bone stimulating factors as insulin like growth factors 1&2, colony stimulating factors, osteoprotegerin, tranforming growth factor-beta.
Estrogen is important hormone both in males & females.
Men with mutation in estrogen receptor alpha have aromatase deficiency grow slowly and have markedly reduced bone densities. Bone mass adjusted for body size is greater in black women than whites.
But they are subject to similar risk factors as thinness, alcohol consumption etc.
Around 75% of bone loss that occurs in women during the first 15yrs after menopause is due to estrogen deficiency rather than to aging it self.
Risk of fracture depends on two factors, the bone mass achieved at maturity and the subsequent bone loss.
The bone density, which is the threshold for vertebral fracture is only slightly lower than the lower limit of normal for premenopausal women.
Changes of bone remodeling
Pathophysiology
Signs and symptoms
Risk factors and investigations
Investigations
Diagnostic tests and biochemical markers
Hormonal treatment
Estrogen modulators, calcium
Vitamin D
Bisphosphonates
Calcitonin, Fluoride, Tibolone
Prevention
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