Arthritis, Osteopenia and Osteoporosis. How Are They Different?
There are many different kinds of bone problems that can cause pain. In this article we review arthritis, Osteoporosis as well as Osteopenia. What are they? what are some of the risk factors, health conditions associated with Osteoporosis and Osteopenia and how to monitor your treatment.
How Are These Bone Conditions Different?
Osteoporosis and osteopenia are both caused by a reduction in bone density, whereas osteoarthritis is a degeneration of a joint due to a breakdown of cartilage. Arthritis is the swelling and tenderness of one or more joints. The main symptoms of arthritis are joint pain and stiffness, which typically worsen with age. Osteopenia is a condition that begins as you lose bone mass and your bones get weaker. This happens when the inside of your bones become brittle. Osteoporosis causes bones to become weak and brittle — so brittle that a fall or even mild stresses such as bending over or coughing can cause a fracture. Osteoporosis-related fractures most commonly occur in the hip, wrist or spine.
Who Is at Risk for Arthritis, Osteopenia and Osteoporosis?
Not everyone develops osteopenia or osteoporosis but there are several risk factors that increase your chances. These include;
- Gender: Women are a higher risk because they have less bone mass than men and we know now that hormones increase the risk for osteoporosis and osteopenia. Women are at greater risk after menopause, but it is important to realize that this bone loss can occur decades before the diagnosis.
- Race: Asian and Caucasian women, especially those who are small-boned, are at highest risk.
- Family history: if you have a family history of osteopenia or osteoporosis you may have a 50%-85% increased risk of developing osteoporosis.
- Age: As we age a lifetime of stressors, poor diet, poor lifestyle habits catch up to us. Diets that lack protein, fat, calcium, vitamin D, Boron Strontium. The average person loses approximately .5% of bone mass every year after the age of 50.
- Lifestyle choices: Destructive habits such as smoking, excessive use of alcohol or caffeine, lack of exercise all increase ones risk for a loss of bone mass.
- Other medical conditions: Hyperthyroidism, Hyperparathyroidism, and Cushing’s syndrome, can contribute to bone loss.
- Medications- Many drugs can affect bone metabolism. As an example, heparin, warfarin, cyclosporine, glucocorticoids, medroxyprogesterone acetate (Birth control pills), cancer drugs, and thyroid hormone can cause bone loss. Prednisone or phenytoin (epileptic medications), are all known to cause bone loss as well.
Facts About Osteoporosis and Osteopenia
- Worldwide, one in three women and one in five men over 50 will experience an osteoporotic fracture
- People who suffer from a hip fracture have a 20% or greater risk of dying during the following year
- One in three adults who lived independently before a hip fracture remain in a nursing home for at least a year after injury
- A 50-year-old woman has a 2.8% risk of death related to hip fracture during her remaining lifetime, equivalent to her risk of death from breast cancer and four times higher than that from endometrial cancer*
*All facts and statistics are based on research studies cited by the International Osteoporosis Foundation www.iofbonehealth.org/facts-statistics
Health Conditions Associated With Osteoporosis:
- Celiac disease
- Inflammatory bowel disease
- Congenital bone disorder
- Anorexia nervosa or other eating disorder in the first 20 years of life.
- Cushings syndrome
- Cystic fibrosis
- Kidney failure
- Rheumatoid arthritis
- Estrogen or androgen deficiency
- C677T polymorphism – genetic studies show an association between the common MTHFR C677T polymorphism and the risk of osteoporosis. C677T polymorphism of the MTHFR gene was associated with BMD of the femoral neck and lumbar spine in postmenopausal women. The women with the TT genotype of MTHFR have lower BMD, which suggests that the TT genotype could be a risk factor for postmenopausal osteoporosis.
- Low Stomach acid – decreases the ability to absorb minerals
- Low diversity of intestinal microbes
- A diet of high oxalate foods – oxalate binds calcium, magnesium and other minerals decreasing their absorption. Oxalates are really high in soy, and next would be spinach.
- A diet of high phytates such as found in grains, beans, nuts, and seeds will also chelate minerals and decrease calcium/magnesium absorption as well as interrupt vitamin D metabolism.
How To Monitor Osteoporosis and Osteopenia
Bone mineral density is a common surrogate marker of osteoporosis treatment efficacy. However, due to the relatively small effect of treatment relative to the precision of the test, it is not practical to repeat bone mineral density testing at intervals shorter than 2 years. Instead, a follow-up test to monitor the bone response in hormone replacement therapy and/or osteoporosis treatment protocols is the Pyrilinks-D testing.
Pyridinium crosslinks consist of both pyridinoline and deoxypyridinoline. Deoxypyridinoline is found predominantly in bone tissue, whereas pyridinoline is found in both bone and cartilage. Pyridinium crosslinks are released when bone is broken down (or resorbed). While not diagnostic of osteoporosis, these markers may be used to monitor bone resorption status and therefore are a useful gauge of treatment efficacy.
The level of deoxypyridinoline (DPD) is elevated, indicating an increased rate of bone loss. In individuals with no underlying bone disease, this is an important marker in the development of osteoporosis. Elevations of DPD may also suggest a recent fracture (levels may stay elevated for up to a year), or a rapid state of bone development as is found in adolescence.
The interplay between bone formation and resorption is a continuous lifelong process which favors bone formation in the early years of life, leading to a peak bone mass at approximately 20 to 30 years of age. From there on, the total bone mass gradually declines in both men and women.
Menopause and Bone Loss
Some women experience an increased rate of bone loss in the early post-menopausal years. The cycle of bone remodeling starts with osteoclasts (resorption cells) eroding bone surfaces, thereby forming cavities. This results in the release of collagen degradation by-products into the circulation system, such as pyridinoline and deoxypyridinoline cross-links, hydroxyproline and N- and C-collogen telopeptides.
At the same time, osteoblasts (bone-forming cells) secrete bone matrix proteins, 90% of which are collagen type I with other minor proteins, as well as the hormone osteocalcin and the bone-specific isoenzyme of alkaline phosphatase and procollagen I extension peptides, which are secreted into general circulation. The final step in the cycle is the mineralization of the matrix protein by calcium salts.
Additional mechanical bone tensile strength is attained by the formation of pyridinuum cross-links (pyridinoline [Pyd] and deoxypyridinoline [DPD]) between the neighboring mature collagen fibrils.
The prolonged course of illness and disability from a chronic disease such as arthritis results in extended pain and suffering and decreased quality of life for millions of Americans.
Read more about treating arthritis and joint pain…
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