What Is Postmenopausal Osteoporosis?

Postmenopausal osteoporosis (PMO) is a common aging-related disease, which mainly occurs in postmenopausal women. Due to estrogen deficiency, bone mass decreases and bone tissue structure changes, increasing bone fragility and easy fracture Fractures cause pain, bone deformation, and comorbidities, which seriously affect the physical health and quality of life of the elderly, and even shorten their lifespan. The prevalence of PMO in postmenopausal women is four times that of men. The osteoporosis is defined by the WHO as having a bone density below 2.5 standard deviations below normal under dual energy X-rays (DEXA).

Basic Information

Visiting department: Obstetrics and Gynecology

Disease characteristics: Humpback, short stature or bone pain
Multiple people: Postmenopausal women

Causes of postmenopausal osteoporosis

Lack of estrogen is one of the main causes of PMO. Estrogen can promote early osteoblast differentiation, stimulate collagen and inhibit osteoclast activity. Postmenopausal severe estrogen deficiency results in increased osteoclast activity, decreased bone density, increased bone turnover, affected calcium salt deposition, increased bone ablation, and a large amount of bone loss, ultimately leading to PMO.

PMO can be divided into two categories: early postmenopausal osteoporosis, characterized by rapid bone loss, and related to the decline of estrogen after menopause; late postmenopause osteoporosis, which occurs 10 to 20 years after menopause, and bone loss Slow, and secondary hyperparathyroidism in the elderly, further worsening PMO.

Clinical manifestations of postmenopausal osteoporosis

Osteoporosis is an insidious disease. Before a fracture does not occur, there are often no symptoms. Once a humpback, short body or bone pain is found, a fracture has often occurred. The main performance is as follows:

Bone pain

Osteoporotic bone pain is usually caused by a microfracture of the trabecular bone. When the position changes, the muscles and ligaments are stretched, so sitting pain, forward and posterior extension pain, walking pain, turning pain, and supine pain can occur .

2. Humpback or short

Appears when a vertebral compression fracture occurs.

3. Local tenderness or throbbing pain

It is characterized by no local swelling and fever.

Postmenopausal osteoporosis

Biochemical indicators of bone resorption

Urinary Ca / Cr, Urinary HOP / Cr: Type I collagen-pyridine cross-linker and terminal peptide, blood anti-tartrate acid phosphatase (TRAP).

2. Bone formation biochemical indicators

Serum alkaline phosphatase (ALP) and bone alkaline phosphatase (bAIP), serum osteocalcin (BGP), and serum type collagen propeptide.

3. Bone mineral density (BMD) measurement

The WHO revised the diagnostic criteria for bone mass measurement in 1994 as BMD, or BMD is 2.5 SD lower than the average of normal adults, and is called the T-score. The calculation method is: (measured BMD-normal adult average BMD) ÷ standard deviation.

4. Bone Ultrasound

The speed, amplitude attenuation, and hardness index (SI) of ultrasound through bone tissue are used to reflect bone structure and bone mass. Some people compare the value of the ultrasound examination with the results of the DXA examination, so they can be used to observe the changes in the condition and the treatment effect.

5. Bone tissue biopsy

Make living bone tissue into sections, observe the structure and morphology under a microscope, and measure bone morphometric indicators such as bone trabecular area, bone trabecular diameter, and osteoid width, which can be used for the differential diagnosis of difficult cases and study bone metabolism situation.

Postmenopausal osteoporosis diagnosis

Bone mineral density (BMD) is a criterion for the diagnosis of osteoporosis. BMD is 2.5 standard deviations or more below the absolute value of premenopausal women.

Postmenopausal osteoporosis treatment

1. Hormone replacement therapy (HRT)

A large number of studies have confirmed that postmenopausal women can prevent bone loss by using estrogen alone or in combination with progestin. There is a clear relationship between estrogen dose and efficacy. Emphasize the use of the lowest effective dose to avoid its side effects. HRT needs to be applied continuously. If it needs to be stopped, other treatments should be added to maintain a beneficial effect on bone mass.

2. Calcium supplement

The recommended daily calcium intake for menopausal women is 1000-1500mg elemental calcium. Prolonged calcium supplementation for elderly women may partially reverse age-related increases in serum parathyroid hormone (PTH) and bone resorption and reduce bone loss. Although calcium supplementation is relatively safe, care should be taken to monitor blood and urine calcium concentrations. If the blood calcium is in the normal range, and the 24-hour urine calcium is between 100 and 200 mg, the dose is appropriate; if the urine calcium is between 300 and 400 mg, it means that the dose of calcium or vitamin D is too large, and it should be reduced; if the urine calcium is> 400 mg, stop taking To avoid kidney or bladder stones.

3. Vitamin D

Daily supplementation of 400U vitamin D3 to elderly women can slightly reduce PTH secretion and increase femoral neck bone density, but the biochemical indicators of bone turnover have not changed. For elderly women at high risk of vitamin D deficiency, such as chronic diseases, lack of outdoor activities, long-term home or elderly people in nursing homes, it is recommended to supplement 400 to 800U of vitamin D daily. Elderly people, due to liver 25-hydroxylase and kidney 1-hydroxylase deficiency, should choose active vitamin D, such as 1 (OH) D3 (Alfadi three), calcitriol [1, 25 (0H) 2D3, Luo calcium whole] and other oral, supplementation effect is better.

4. Bisphosphonate diphosphate

It is a powerful bone resorption inhibitor developed in the 1950s, used to treat diseases with accelerated bone resorption, such as deformable osteitis (Pagets disease), malignant tumor bone metastasis and its accompanying hypercalcemia. The effect is best when the bone turnover is accelerated, so it is also suitable for postmenopausal osteoporosis.

5. Calcitonin (CT)

Calcitonin includes eel calcitonin, procalcin, salmon calcitonin, and dense calcitonin. Binding to osteoclast membrane surface receptors activates adenylate cyclase to increase CAMP and activates the phospholipid inositol system to increase cytosolic free calcium. Both effects inhibit osteoclast resorption, increase bone mass, and have significant analgesic effects.

6. Selective estrogen receptor modulator (SERM)

SERM is a class of synthetic estrogen-like compounds that selectively act on estrogen receptors in different tissues, producing estrogen-like or anti-estrogen effects, respectively. Raloxifene and tamoxifen (tamoxifen) have a better effect on bone mass and blood lipids, but the clinical application prospects of raloxifene are more promising.

7. Parathyroid hormone (PTH)

Small-dose subcutaneous injection of PTH has osteogenesis in animal experiments, which can increase bone mass and improve anti-fracture ability. At present, there are few clinical application data, and further clinical observation and research are needed.

Prognosis of postmenopausal osteoporosis

Among the serious complications caused by postmenopausal osteoporosis, 12% to 14% of hip fractures died from various complications of the circulatory, respiratory, and digestive systems within one year after the fracture. 50% of survivors have limited mobility.