Introduction:
Osteoporosis is a prevalent and complicated medical condition that affects postmenopausal women, particularly the elderly. It is a degenerative skeletal illness that shows signs of decreasing bone mineral density (BMD) and collateral damage to the bone microarchitecture. As a result, the skeletal system may become weaker and more prone to fractures. According to statistics, more than 50% of persons 50 or older have osteoporosis, with postmenopausal women making up over 70 % of this group. The use of BMD as a substitute measure for the diagnosis of osteopenia and osteoporosis is generally recognized. BMD is useful as a diagnostic tool for abnormal bone mass and osteoporosis since a person is clinically deemed to have osteoporosis if their BMD is more than 2.5 standard deviations (SD) below the adult mean value. Several different variables, including specific nutrients like calcium and vitamin D, coffee, alcohol, body weight, physical activity, and exercise, are linked to BMD. According to a prior study, body weight and body mass index (BMI) has the most effects on postmenopausal women's BMD among these variables.
What Is The Correlation Between Bone Mineral Density And Bone Mass Index?
Lean mass (LM) and fat mass (FM) comprise most of a person's body weight, with FM making up the remaining 16 % to 25 % of a normal-weight person's total body weight. Males have a stronger association between LM and BMD than females, and postmenopausal females have a stronger effect of FM on BMD than premenopausal females. In earlier research, body FM has been identified as the most important predictor of BMD in postmenopausal women. However, other research proved that LM and FM are connected to bone mass.
The BMI formula determines how much tissue mass (muscle, fat, and bone) an individual has. This figure is used to classify an individual as underweight, normal weight, overweight, or obese. In prior research, increased BMI has been shown to have a protective effect on bone density. In addition, those who are moderately overweight were shown to have elevated BMD values, suggesting that BMI and weight growth may be related to BMD. More importantly, it has been shown that gaining weight is associated with endocrine changes that can either directly or indirectly have a favorable impact on bone metabolism.
Low body weight or BMI is believed to predispose postmenopausal females to fast bone loss and poor bone density, which are considered key factors in the pathophysiology of postmenopausal women's osteoporosis. However, there is more work to properly build a BMI value chart that can reliably forecast osteoporosis and the risk of corresponding fractures. According to early findings, BMI between 26 and 28 may offer some protection. However, having a BMI between 22 and 24 puts you at higher risk.
What Are the Diagnosis Basis of Bone Diseases?
1) Osteoporosis (OP):
A skeletal metabolic illness called osteoporosis, which has a variety of origins, is characterized by bone loss, microstructure deterioration, increased brittleness, decreased bone strength, and an elevated risk of fracture. As a result, OP negatively impacts patients' quality of life and level of living. Indicators such as bone mineral density are frequently utilized to diagnose OP using dual-energy X-ray bone absorptiometry (DEXA). BMD can also be used to monitor OP changes and assess the effectiveness of OP medications. Numerous studies strongly imply that metabolic syndrome (MS), which includes abdominal obesity, hypertension, dyslipidemia, and dysglycemia, is connected to OP. Because obesity is linked to greater amounts of 17-estradiol and higher mechanical stresses, which may protect bones, enhancing bone density.
2) Vitamin D:
Because of its capacity to control calcium and phosphorus absorption, vitamin D is believed to play a significant role in the body's growth and maintenance of bones and muscles. Low vitamin D levels are thought to increase the risk of osteoporosis and bone fractures. A lack of serum vitamin D eventually causes high levels of parathyroid hormone (PTH) release by preventing the digestive tract from absorbing Ca2+ from food. PTH overproduction maintains healthy blood levels of the minerals, calcium, and phosphorus needed for metabolic processes and neuromuscular function while also causing the creation of osteoclasts and inhibiting osteogenesis.
3) Rheumatoid arthritis (RA):
The most prevalent inflammatory arthritis is rheumatoid arthritis (RA), a chronic, systemic autoimmune illness marked by intense, symmetrical inflammation of several joints. According to epidemiological research, 90% of RA patients experience bone erosion within two years of the disease's inception, which can lead to joint deformities or possibly disability. As a result, RA has caused tremendous pain and suffering for patients, their families, and even the entire society. Type 2 diabetes and RA are two chronic autoimmune and inflammatory illnesses that are more common in those who are overweight or obese. There is proof that a higher BMI is linked to a higher chance of developing RA. TNF-, IL-1, IL-6, IL-8, and MMP production are proinflammatory mediators induced by visfatin and are characteristic signs of RA joint inflammation. Similarly, adiponectin induced the production of IL-6, IL-8, and PGE2 by fibroblast-like synoviocytes (FLS) in RA patients. Adiponectin also boosted VEGF and MMP synthesis in RA FLS, which might lead to inflammation and joint damage.
4) Osteoarthritis (OA)
The most prevalent degenerative joint affecting older people, notably the knee joint, is osteoarthritis (OA). Articular cartilage gradually deteriorates in OA, and the synovial membrane, knee meniscus, adipose tissue, periarticular ligaments, and subchondral bone undergo structural alterations. Age-related OA is linked to various variables, including age, sex, trauma, and obesity, according to clinical and animal research. The most significant and reversible risk factor among these is obesity.
Mounting evidence points to a direct connection between fat and inflammation. It has been demonstrated that adipose tissue controls cartilage's inflammatory and immunological responses.
5) Hormone Related:
In comparison to the normal weight group or the overweight group, the BMD in the postmenopausal ladies' lumbar vertebra (L1-L4), femoral neck, proximal femur, and Ward's triangle region was considerably lower in the underweight group. Interesting to see, BMD rose as BMI rose. When taken as a whole, these findings revealed that BMD is significantly influenced by both body weight and BMI. The primary multiple processes, according to our conjecture, involve mechanical load, hormones, and nutritional condition. According to a previous study, larger body weight and BMI give people the ability to withstand greater mechanical loads, which reduce bone resorption and stimulate bone formation. This increases bone strength and bone mineral content, delays the onset of osteoporosis, and lessens the severity of the condition. The synthesis of sex hormone-binding globulins is also diminished in postmenopausal females with greater BMI, which results in higher amounts of free sex hormones. Estrogens activate the estrogen receptors on osteoblasts, increasing the production of osteoprotegerin and reducing osteoclast activity and bone resorption as a result. In addition, estrogens encourage bone growth and stop parathyroid hormones from being absorbed into the bones.
Conclusion:
Factors including body weight and BMI significantly influence BMD. Low BMI postmenopausal ladies have osteopenia and are more susceptible to osteoporosis development. Thus, BMI can be used as a key indicator to stop osteoporosis. It may be required to regularly assess BMD in postmenopausal females who are underweight to decide whether to start early therapeutic therapies for osteoporosis.
