- What You Need to Know About Osteoporosis
- Bone Remodeling and Osteoporosis
- Who Is Affected by Osteoporosis
- Osteoporosis is ‘Silent’ Until it Hurts
- Does Osteoporosis Cause Leg Pain?
- Chronic Pain, Osteoporosis, and Bone Density Testing
- Osteoporosis and Non Specific Chronic Low Back Pain: Correlation with Sex and Severity of Backache
What You Need to Know About Osteoporosis
Osteoporosis is a condition of low bone density and structural deterioration of bone tissue that causes an increased risk of fractures. Osteoporosis on its own does not cause pain or obvious symptoms. Complications from the condition, including vertebral fractures, may result in back pain and limited mobility.
Osteoporosis can lead to vertebral compression fractures – injuries that occur when bone tissue inside the vertebrae of the spine breaks and then collapses. Read Osteoporosis: The Primary Cause of Collapsed Vertebrae
More Osteoporosis Info
To catch osteoporosis early, as well as to identify those at risk of fractures caused by the condition, screening for risk factors is advised on the basis of age and sex. If screening identifies a relatively high risk for osteoporosis, a bone density test (densitometry) may be ordered.
In general, all women over age 65 and younger postmenopausal women with risk factors should be screened for low bone density. Some recommendations call for women to be screened as early as age 50.1 While there is no official recommendation in the U.S. for men, who are less at risk, it is generally advised that men over 70 are screened.1
See Osteoporosis in Men
Bone Remodeling and Osteoporosis
Bone is formed through a different process than most other tissues in the body that grow by cells dividing in two. Instead, bone undergoes a continuous process of breaking down old cells and building new cells in their place. Osteoporosis occurs when bone breaks down faster than it can reform, leading to depleted bone density.
The process of bone growth is called remodeling. Bone remodeling consists of the following:
- First, large cells called osteoclasts release enzymes that break down existing bone cells.
- Fragmented bone cells are processed (or “digested”) in the osteoclast.
- The calcium and phosphorus from the fragmented bone cells are released into the bloodstream in a process called resorption.
- Other cells called osteoblasts produce a variety of enzymes, growth factors, and hormones that create a matrix of cells in a process called bone formation.
- The osteoblasts are absorbed into the matrix and become osteocytes (bone cells).
Most people reach peak bone mass between ages 18 and 25,2 when bone remodeling and resorption occur at about the same rate. As a person ages, the hormones that influence bone remodeling and resorption tend to change and more bone is broken down than can be rebuilt.2
In This Article:
Who Is Affected by Osteoporosis
Osteoporosis is one of the most common issues leading to back pain in the U.S. Roughly 500,000 spinal fractures occur due to osteoporosis every year.3
See Osteoporosis: The Primary Cause of Collapsed Vertebrae
Because bone growth naturally slows down later in life, osteoporosis can affect both men and women over age 50. The largest population affected by osteoporosis is postmenopausal women.
See Why Women Are at Greater Risk for Developing Osteoporosis
Transgender men and women taking hormone replacement therapy may be at increased risk of osteoporosis if they skip or stop taking hormones.4 However, very little transgender health research has been conducted to determine if transgender people in general have a higher risk for osteoporosis.4
The TOH has been reported more frequently in healthy middle-aged males with a male:female ratio of 3:1.7,8 Although lesser in females it is more commonly seen in pregnant women in their third trimester, has also been reported in nonpregnant women without any previous history of infection or trauma.9
The exact etiology of this condition is still unknown, and some theories have been proposed, explaining this condition. The etiopathogenesis of TOH may include microvascular injury, nontraumatic reflex sympathetic dystrophy, metabolic, viral infection, neurological, and endocrine factors.10 Curtiss and Kincaid advocated a neurogenic hypothesis, child’s head compressing mother’s obturator nerve, as one of the contributory factors of TOH. Viral infection simulating an increased osteoclastic bone resorption, resulting in hip pain because of stress fractures in femoral head was proposed as a possible etiological factor.11 BME surrounding the femoral hip has led to believe in the theory of ischemia as one of the underlying causes. According to some researchers, this is due to a disturbance of the venous drainage.12 This theory is also supported by angiographic and scintigraphic studies, showing dilated nutrient vessels of the femoral head resulting an increased perfusion in the affected area, suggesting ischemia as a causative factor.13 Due to these associated findings, various acronyms of TOH have been proposed including “bone marrow edema syndrome” or “transient osteoporosis of the hip.”14 A transient ischemic episode leading to a contained area of cell necrosis was thought to be the cause of TOH.15 It was described as an early reversible phase of other mimicking pathology, i.e., avascular osteonecrosis of the hip.16 Some authors believe TOH to be a nontraumatic type of CRPS, because of its striking resemblance in various clinical, radiological findings of both these pathologies. However, TOH lacks specific cutaneous changes that are characteristic of reflex sympathetic dystrophy,17 which may be due to the deep location of the hip joint. We believe that TOH could be a subset of CRPS, as it has many similarities with it, namely, an unknown cause, characteristic pain (which is usually out of proportion to the physical and radiological findings), vasomotor dysfunction of the extremity and it develops in the absence of an identifiable precipitating event. TOH need to be differentiated from other similar clinical conditions such as avascular necrosis , insufficiency fracture, infective, and inflammatory arthritis.
Radiological differentiation between transient osteoporosis of hip and avascular necrosis
The onset of pain in TOH is sudden and more severe than osteonecrosis. Clinically, it presents as a dull aching pain in the groin region, buttocks, or anterior aspect of the thigh. It is frequently accompanied by limp and an antalgic gait. The pain is worse in the night and on weight bearing. Functional disability is often disproportionate to the symptoms as described by Lequesne,2 with preservation of a range of movement. Occasionally, there may be some limitation of abduction and rotation. The TOH usually affects a single, but in sporadic cases, bilateral involvement has also been reported, similar to 2/12 cases in this series. Xyda et al.18 reported bilateral TOH in 3 cases in postpartum females.
Three distinct phases of TOH are known.19 The initial phase is defined by a sudden onset of pain associated with functional limitation lasting for 1 month. It is followed by a phase of which sign and symptoms follows a consistent trend with no further aggravation of pain and lasts for about 1–2 months. During this stage, osteopenia is a specific finding on routine radiographs. The final phase is characterized by spontaneous regression of clinical sign and symptoms and the bone density returning to normalcy; this period is usually as long as 4 months.
The radiographic features often lag behind clinical symptoms by 1–2 months. Initial X-rays show focal osteopenia involving femoral head and neck region. As the disease progresses, there might be complete effacement of the subchondral cortex of femoral head, and sometimes, a near absence of the osseous architecture, thereby creating an optical void known as phantom appearance’ of the femoral head. Characteristically, during the whole course of the disease, there is the preservation of joint space with no osseous erosion or subchondral collapse, similar to our experience in this study. A bone scan is sensitive, but a nonspecific test. However, it can be a valuable screening tool for an early diagnosis of TOH. There is an increased uptake with radioisotope bone scanning even before radiographic changes are visible, thereby helping in early diagnosis of the pathology. Bone scintigram is characterized by an increased uptake in all the three phases indicating a focal area of hyperemia and increased capillary permeability with an increase in osteoblastic activity. Knees, or the shoulders. Radionuclide scanning provides an efficient screening tool for the entire body, and it may also reveal the asymptomatic involvement of other body parts such as the contralateral hip. An MRI is a very sensitive test to diagnose TOH and was described first in the radiology literature by Bloem.20 T1-weighted images demonstrate low signal intensity, and the T2-weighted images reveal matching high intensity involving femoral head to the intertrochanteric region, usually associated with effusion. MRI also helps in ruling out other pathologies such as avascular necrosis, insufficiency fractures, infection, and neoplasm which mimic TOH .
Differential diagnosis of transient osteoporosis of hip and their distinguishing features
TOH is a self limiting disease, a symptomatic and supportive treatment is recommended, which includes the use of NSAIDs with protected weight bearing and graduated physiotherapy regime.21,22 In an acute phase, intermittent traction helps in preventing and simultaneous correction of deformity associated with a joint effusion. Although nonweight bearing is advantageous on the affected joint in long duration, this may lead to disuse demineralization. Trevisan23 advocated densitometric analysis in the conservative treatment of TOH. Physiotherapy regime must include abductor strengthening exercise and preservation of a range of hip movements. In this study, the average time for resolution of symptoms was 17.1 weeks. Of the 12 cases reported, 2 cases had a period of complete resolution of >20 weeks (23 and 25 weeks). The possible reason could be bilateral involvement, which led to delayed mobilization and rehabilitation protocol.
Several authors have discussed the beneficial role of various therapeutic agents such as bisphosphonate (both oral and intravenous), as effective means of treatment and may also speed up the recovery.24 Calcitonin in the form of a nasal spray (200 IU daily) has also been described,25 to reduce the bone loss during the acute phase of the disease. Iloprost (a prostacyclin analog) has been used recently with the satisfactory outcome with painful BME of the knee joint.26 Pain management and rapid regression of pathology are due to prostacyclin properties, dilating blood vessels and also reducing the permeability of small vessels (capillaries). Its effectiveness in TOH is still under consideration. The various studies which have described the role of various pharmacological agents such as calcitonin and bisphosphonates are based on small case series and sample size.24,26 The absence of a series with a large sample size can be attributed to the rare incidence of the disease along with delay in diagnosis of the disease, due to it closely mimicking avascular necrosis. To assess the role of these pharmacological agents in TOH, large-scale studies with control groups are needed.
Osteoporosis is ‘Silent’ Until it Hurts
Your experience with pain and its resolution are unique, so don’t compare your pain with that of a friend who has been through a similar procedure or event. And remember, says Fortman, that your willingness to actively participate in pain management directly affects your success in easing pain symptoms.
Does Osteoporosis Cause Leg Pain?
Q1. I’m menopausal, and I was told that I have osteoporosis. I also have upper leg pain. It is hard for me to walk or stand very long. What is causing the pain in my legs, and what can I do for the pain?
Osteoporosis a condition of your bones where they are thin and subject to increased risk for fracture. This is often just a result of aging, but can lead to considerable disability, especially when associated with back and hip fractures. However, osteoporosis does not usually cause pain unless you have a fracture. And it is unlikely that the leg pain you describe is from osteoporosis.
So your first step is to make a diagnosis. Is this musculoskeletal pain, nerve pain or joint pain? Visit your doctor to discuss your symptoms in greater depth and figure out what’s causing the pain. Each of these types of pain will require a different treatment approach.
Q2. I am lactose intolerant. I also have osteoporosis. Readings suggest that vitamin D is not absorbed by those who are lactose intolerant. What can I do to raise my level of calcium and vitamin D absorption?
Lactose intolerance can be associated with loose stools, diarrhea, and poor absorption of most micronutrients (not just vitamin D). To avoid these digestive problems, steer clear of dairy products with lactose, use Lactaid before eating dairy, or stick with Lactaid-treated products.
While dairy products are high in calcium, and many are fortified with vitamin D, there are many sources of calcium and vitamin D that don’t involve dairy. These include sardines, tofu, and calcium- and vitamin D-fortified soy milk or orange juice. You can add these foods to your diet, if you’re not already eating them.
The real answers to your problem, though, are calcium and vitamin D supplements. You can take calcium with vitamin D or buy a separate vitamin D supplement. You want to get 600 to 800 IU of vitamin D total each day. The current guidelines actually call for 400 IU daily, but this is probably lower than what is needed. Most multivitamins contain 400 IU of vitamin D, so take an additional vitamin D supplement if you take a multi. Sunlight and UV exposure also increase vitamin D synthesis in the skin, but there’s a delicate balance between getting adequate UV exposure and avoiding skin cancer.
I can’t say exactly what your daily calcium intake should be, as it’s not clear what your age is, but aim for at least 1,000 mg, if not 1,200 mg, of calcium a day. Be sure to take no more than 500 mg of calcium at a time, though. Our bodies have a hard time absorbing large amounts of calcium at once, so it’s better to take spread your dosage throughout the day. There are many different types of calcium on the market, but some studies have shown that calcium citrate may be better absorbed and tolerated by some women.
Q3. I am 58 years old, and I have mild osteoporosis. I tried taking Actonel, but it destroyed my esophagus. The results of my last test came back, though, and my osteoporosis is getting worse. My internist doctor suggested that I take Boniva (150 mg), but my gynecologist says no. I don’t know what to do, and I am worried that I will have a problem with Boniva. Any suggestions?
— Miriam, New York
I would recommend avoiding any of the bisphosphonate drugs that you take orally (by the mouth), as they can irritate the esophagus. These include drugs such as Actonel (which you already tried), Boniva, and Fosamax. The Boniva your internist suggested is a pill that you take once a month orally. However, the U.S. Food and Drug Administration (FDA) very recently approved a version of Boniva that is given by injection once every three months. It also provides bone benefits and isn’t likely to affect your esophagus. You should talk to your doctors about this option.
If you want to avoid bisphosphonate-type drugs altogether, there are other medications you can take for bone protection. For example, there’s calcitonin, an FDA-approved hormone that comes from several animal species, with salmon calcitonin being the most widely used. There’s also Forteo, a synthetic version of parathyroid hormone, which helps regulate calcium metabolism and promotes the growth of new bone.
There are many options out there, so talk to your doctors about the injectable form of Boniva and other potential treatments. If they don’t feel comfortable prescribing you a new medication, you may want to get a referral to an endocrinologist who specializes in osteoporosis to review newer treatment options.
Q4. I am a 53-year-old postmenopausal woman. My first bone density test showed that I have osteopenia, but my most recent one indicates that the osteopenia is stable. I’m taking 1,500 mg of calcium and 800 units of vitamin D daily. My doctor told me I don’t need to take osteoporosis drugs such as Fosamax or Boniva, but I thought bone loss was a big problem the first five to seven years after menopause. Why would she recommend this?
— Mary, Massachusetts
There’s a lot of controversy over whether women should take low-dose osteoporosis drugs (such as Fosamax) when they have osteopenia, because women can end up being on the drugs for decades. Some doctors believe in prescribing a low dose of these bisphosphonate drugs for preventive purposes to women with osteopenia, but it has not been well established that this is the best way to proceed. I generally don’t recommend this route unless someone is creeping very close to osteoporosis. If you’re right on the border, it may be reasonable to start medication, but I’m not sure your osteopenia falls into that category. Remember that no drug is without costs or risks. Talk with your doctor about whether taking this kind of drug makes sense for you.
In the meantime, you can also get good results with lifestyle changes. Be sure to take 1,200 mg of calcium and 800 IU of vitamin D daily (congrats, because you’re already getting a good amount!). Also, be sure to do weight-bearing exercise at least 30 minutes a day and resistance training for 20 minutes two to three times a week. Finally, avoid smoking, excessive caffeine or alcohol, and large quantities of carbonated beverages. These changes can go a long way toward preventing osteopenia from progressing into osteoporosis
Learn more in the Everyday Health Osteoporosis Center.
Chronic Pain, Osteoporosis, and Bone Density Testing
Bone density testing in chronic pain patients can diagnose osteoporosis and identify those at high risk for fracture so that appropriate therapy can be initiated to reduce future fracture risk. By E. Michael Lewiecki, MD, FACP
Osteoporosis is a disease manifested by low bone density and poor quality of bone, resulting in skeletal fragility and increased risk of fracture.1 While osteoporosis is generally a silent and asymptomatic disease until a fracture occurs, pain and osteoporosis are often associated. Fractures usually cause sudden and severe pain, with non-union fractures and some vertebral fractures resulting in chronic pain. Recent evidence suggests that pressure-induced tibial pain may be an indicator of low bone density in patients without fracture.2 Some metabolic disorders that cause low bone density, such as vitamin D deficiency and osteomalacia, can cause bone and muscle pain,3 proximal muscle weakness, and postural instability4 in the absence of fracture. Chronic pain is associated with many risk factors for osteoporosis and fragility fractures. These risk factors may be categorized according to whether they are due to the underlying disease, the pain itself, or the treatment for pain (see Table 1).
Diseases associated with chronic pain and osteoporosis include prevalent vertebral fracture, rheumatoid arthritis, inflammatory bowel disease, multiple myeloma, and insulin-dependent diabetes5 with diabetic neuropathy. Regional bone loss may occur with painful disorders such as reflex sympathetic dystrophy6 (Sudeck’s atrophy, algodystrophy) or immobilization of a limb due to trauma — with or without fracture.7
Chronic pain and its associated diseases may result in poor nutrition, impaired cognition, elevated serum cortisol8 or high levels of inflammatory cytokines,9 with potential adverse effects on bone density.
Some treatments for chronic pain disorders, such as glucocorticoids10 and anticonvulsants,11 may be harmful to bone. Other medical treatments, such as narcotics and antidepressants, may impair balance and mobility, resulting in increased risk of falls and fractures.12 Hypogonadism, another risk factor for osteoporosis, has been reported in men13 and women14 treated with opioids.
The consequences of a fracture may include additional acute and chronic pain, limited ambulation, disability, loss of independence, increased risk of future fractures and death.15 Chronic pain patients at risk for osteoporosis should be considered for bone density testing so that appropriate therapeutic intervention may be started to prevent fractures and their clinical consequences.
“…dual-energy X-ray absorptiometry (DXA) of the spine and hip is the recommended method for diagnosing osteoporosis and monitoring the effects of therapy.”
Bone Density Testing
Bone density testing is a non-invasive technique used to diagnose osteoporosis or low bone density, predict the risk of fracture, and monitor the effectiveness of therapy for osteoporosis. While measurement of bone density at peripheral skeletal sites with a variety of technologies is useful to increase osteoporosis awareness and predict fracture risk, dual-energy X-ray absorptiometry (DXA) of the spine and hip is the recommended method for diagnosing osteoporosis and monitoring the effects of therapy. The key to effective clinical management is the identification of high risk patients before the first fracture occurs, so that therapy can be initiated to reduce the risk of fracture.
Dual-energy X-ray Absorptiometry
DXA is used to measure bone mineral density (BMD) at the spine and proximal femur. With appropriate software, many DXA instruments can also measure BMD at the forearm and total body. DXA measures areal BMD (aBMD in g/cm2) by using ionizing radiation with photon beams of two different energy levels. DXA is the “gold-standard” method for the diagnosis of osteoporosis and monitoring the effects of therapy for the following reasons:
- biomechanical studies have shown a correlation between mechanical strength and BMD measured by DXA,16
- epidemiological studies have established a strong relationship between fracture risk and BMD measured by DXA,17
- the World Health Organization (WHO) classification of BMD for the diagnosis of osteoporosis and osteopenia is based on reference data obtained by DXA,18
- randomized clinical trials showing a benefit with pharmacologic intervention have selected subjects based on low BMD measured by DXA,19
- there is a relationship between reduction in fracture risk with pharmacologic therapy and BMD increase as measured by DXA,20
- the accuracy and precision of DXA is excellent.21
DXA is widely available in the United States, with an estimated 10,000 instruments in operation. Radiation exposure from DXA is extremely small,22 typically about the same as the normal daily level of background radiation. Conventional radiography, on the other hand, is an insensitive and subjective technique for evaluating bone density at any skeletal site, requiring 30-40% bone loss before a problem is detected. The best use of standard X-ray in the management of osteoporosis is to diagnose fractures, to monitor the healing of fractures, and to evaluate for some secondary causes of osteoporosis. If an X-ray is suggestive of low bone density, a quantitative measurement of BMD by DXA should be done.
When to Order a Bone Density Test
As with any clinical test, bone density measurement should only be done when the potential benefits outweigh the risks, and when the results are likely to play a role in making patient management decisions. The risks of bone density testing are extremely low. Pregnancy should be considered an absolute contraindication to doing any X-ray-based bone density test. Many organizations have developed guidelines to aid in the selection of those at risk for low BMD who most likely to benefit from knowledge of the results. The most comprehensive guidelines are those of the International Society for Clinical Densitometry23 upon the recommendation of an international panel of experts (see Table 2).
Due to Underlying Disease
Insulin Dependent Diabetes Mellitus
Inflammatory Bowel Disease
Reflex Sympathetic Dystrophy
Due to Effects of Pain
Due to Pain Treatments
Diagnosis of Osteoporosis
A clinical diagnosis of osteoporosis may be made in a patient with a fragility fracture, provided other causes of fracture have been excluded. A fragility fracture is usually defined as a fracture resulting from a fall from the standing position. It is preferable, however, to identify patients at high risk for fracture before the first fracture occurs, just as risk factors for stroke and myocardial infarction should be identified and managed before a critical event occurs. The World Health Organization (WHO) classification of BMD uses the standard deviation (SD) difference between the patient’s BMD and the mean BMD of a young healthy population (Table 3). This is usually expressed as a T-score, which is calculated by subtracting the mean BMD of the reference population from the patient’s BMD and dividing by the SD of the reference population. A T-score of -2.5 or less is used for a densitometric diagnosis of osteoporosis in a postmenopausal woman.
“If a fracture has occurred, the goal of therapy is to stabilize the fracture, relieve pain, return the patient to pre-fracture levels of activity as soon as possible, and prevent future fractures.”
BMD and Fracture Risk
There is an exponential relationship between BMD and fracture risk, with fracture risk approximately doubling for every 1 SD decrease in BMD.24 Low bone density at any skeletal site is predictive of fractures at any skeletal site although, in general, site-specific fracture risk is best predicted by BMD measurement at that skeletal site. This principle does not hold true with spine BMD and spine fracture risk in the elderly, who often have degenerative arthritis in the spine that may result in an artifactual increase in spine BMD. There is no “fracture threshold.” Instead, there is a continuous relationship between BMD and fracture risk, so that fracture risk is never zero, regardless of how high the BMD, and it is never certain that a fracture will occur, regardless of how low the BMD. In clinical practice, patient management decisions must consider factors in addition to BMD that may affect fracture risk. The most important of these non-BMD risk factors are age25 and previous fracture.26 Fracture risk increases with age, even when BMD remains the same. Other clinical risk factors, such as family history of hip fracture, poor health, low body weight, and frailty, play a role as well. Since most hip fractures occur as a result of a fall, frailty and falling are potent predictors of hip fracture, independent of bone density. The risk of falling is affected by factors that include balance, mobility, strength, reaction time, visual impairment, medications, and cognitive impairment.
When to Repeat a Bone Density Test
A bone density test should be repeated when the expected amount of change in bone density equals or exceeds the Least Significant Change (LSC) — if knowledge of this change is likely to influence clinical management. The LSC is established for each technologist for each instrument used according to well-established guidelines,27 and is best expressed as an absolute value (g/cm2) with a 95% level of confidence. Values for precision error supplied by the manufacturer of the DXA instrument, which are automatically included on some computer printouts, are generally more optimistic than what is achievable in bone densitometry centers and should not be used. It is reasonable to repeat a DXA study 1-2 years after starting pharmacologic therapy to be sure that BMD is stable or increasing, and then repeat the study at intervals of 2 or more years to assure continuing response to therapy. In patients at risk for rapid bone loss, such as those being started on high dose glucocorticoid therapy, it is appropriate to repeat the DXA study every 6 months until stable. For elderly patients in whom a typical age-related bone loss of 0.5-1.0% per year is expected, it may take 3-6 years before a statistically significant change in BMD can be detected.
Indications for Bone Density Testing
- Women aged 65 years and older.
- Postmenopausal women under age 65 years with risk factors for osteoporosis.
- Men aged 70 years and older.
- Adults with fragility fracture.
- Adults with a disease or condition associated with low bone mass or bone loss.
- Adults taking medication associated with low bone mass or bone loss.
- Anyone being considered for pharmacological osteoporosis therapy.
- Anyone being treated for low bone mass to monitor treatment effect.
- Anyone not receiving therapy in whom evidence of bone loss would lead to treatment.
Women discontinuing estrogen should be considered for bone density testing according to the indications listed above
Implications for Therapy
Non-pharmacologic therapy for patients at risk for osteoporosis and fragility fracture includes regular weight-bearing exercise as tolerated; good nutrition with adequate daily intake of protein, calcium, and vitamin D; balance training, fall prevention, and hip protectors for those with high risk of falling; and avoidance of bone toxic agents, such as cigarette smoking and excess alcohol. Pharmacologic therapy with FDA-approved agents can be expected to stabilize or increase BMD, and reduce the risk of fragility fractures by approximately 50%.28 If a fracture has occurred, the goal of therapy is to stabilize the fracture, relieve pain, return the patient to pre-fracture levels of activity as soon as possible, and prevent future fractures. Vertebroplasty and Kyphoplasty may offer pain relief for selected patients with vertebral fractures, although the indications for these procedures and the long-term benefits and risks are not well defined.29
|Normal||-1.0 or greater|
|Osteopenia||Between -1.0 and -2.5|
|Osteoporosis||-2.5 or less|
|Severe Osteoporosis||-2.5 or less with a fragility fracture|
Patients with chronic pain may be at increased risk for osteoporosis and fragility fractures due to the underlying disease or disorder causing the pain, as well as factors associated with the pain itself and treatments given for the pain. BMD testing is an essential tool for the early diagnosis of osteoporosis or low bone density, allowing for identification of high risk patients and selection of appropriate therapy. Currently available therapy can reduce the risk of future fracture and its clinical consequences.
- 1. Klibanski A, Adams-Campbell L, Bassford T et al. Osteoporosis prevention, diagnosis, and therapy. JAMA. 2001 February 14. 285(6):785-95.
- 2. Birtane M, Tuna H, Ekuklu G, Demirbag D, Tuna F, and Kokino S. Pressure-induced pain on the tibia: an indicator of low bone mineral density? J Bone Miner Metab. 2004. 22(5):456-61.
- 3. Plotnikoff GA and Quigley JM. Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc. 2003 December. 78(12):1463-70.
- 4. Pfeifer M, Begerow B, Minne HW et al. Vitamin D status, trunk muscle strength, body sway, falls, and fractures among 237 postmenopausal women with osteoporosis. Exp Clin Endocrinol Diabetes. 2001. 109(2):87-92.
- 5. National Osteoporosis Foundation. Physician’s guide to prevention and treatment of osteoporosis. Washington, D.C. National Osteoporosis Foundation. 2003.
- 6. Quek ST and Peh WC. Radiology of osteoporosis. Semin Musculoskelet Radiol. 2002 September. 6(3):197-206.
- 7. Minaire P. Immobilization osteoporosis: a review. Clin Rheumatol. 1989 June 8. Suppl 2:95-103.
- 8. Tennant F and Hermann L. (229) serum cortisol concentrations and adrenal reserve may be altered by severe chronic pain. Pain Med. 2001 September. 2(3):252.
- 9. Okada Y and Tanaka Y. Immune signals in the context of secondary osteoporosis. Histol Histopathol. 2004 July. 19(3):863-6.
- 10. Manelli F and Giustina A. Glucocorticoid-induced osteoporosis. Trends Endocrinol Metab. 2000 April. 11(3):79-85.
- 11. Farhat G, Yamout B, Mikati MA, Demirjian S, Sawaya R, and Fuleihan GE. Effect of antiepileptic drugs on bone density in ambulatory patients. Neurology. 2002 May 14. 58(9):1348-53.
- 12. Ensrud KE, Blackwell T, Mangione CM et al. Central nervous system active medications and risk for fractures in older women. Arch Intern Med. 2003 April 28. 163(8):949-57.
- 13. Daniell HW. Hypogonadism in men consuming sustained-action oral opioids. J Pain. 2002 October. 3(5):377-84.
- 14. Finch PM, Roberts LJ, Price L, Hadlow NC, and Pullan PT. Hypogonadism in patients treated with intrathecal morphine. Clin J Pain. 2000 September. 16(3):251-4.
- 15. Cooper C. The crippling consequences of fractures and their impact on quality of life. Am J Med. 1997. 103 (2A):12S-9S.
- 16. Lotz JC, Cheal EJ, and Hayes WC. Fracture prediction for the proximal femur using finite element models: Part I—Linear analysis. J Biomechan Eng. 1991. 113:353-60.
- 17. Marshall D, Johnell O, and Wedel H. Meta-analysis of how well measures of bone mineral density predict occurrence of osteoporotic fractures. BMJ. 1996 May 18. 312(7041):1254-9.
- 18. Kanis JA and the WHO Study Group. Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. Osteoporos Int. 1994. 4:368-81.
- 19. Cranney A, Tugwell P, Wells G, and Guyatt G. Systematic reviews of randomized trials in osteoporosis: Introduction and methodology. Endocr Rev. 2002 August. 23(4):497-507.
- 20. Wasnich RD and Miller PD. Antifracture efficacy of antiresorptive agents are related to changes in bone density. J Clin Endocrinol Metab. 2000 January. 85(1):231-6.
- 21. Mazess R, Chesnut CH, III, McClung M, and Genant H. Enhanced precision with dual-energy X-ray absorptiometry. Calcif Tissue Int. 1992 July. 51(1):14-7.
- 22. Genant HK, Engelke K, Fuerst T et al. Noninvasive assessment of bone mineral and structure: state of the art. Journal of Bone & Mineral Research. 1996 June. 11(6):707-30.
- 23. Leib ES, Lewiecki EM, Binkley N, and Hamdy RC. Official positions of the International Society for Clinical Densitometry. J Clin Densitom. 2004. 7(1):1-6.
- 24. Faulkner KG. Bone matters: are density increases necessary to reduce fracture risk? Journal of Bone & Mineral Research. 2000 February. 15(2):183-7.
- 25. Kanis JA, Johnell O, Oden A, Dawson A, De Laet C, and Jonsson B. Ten year probabilities of osteoporotic fractures according to BMD and diagnostic thresholds. Osteoporosis International. 2001 December. 12(12):989-95.
- 26. Aoyagi K, Ross PD, Orloff J, Davis JW, Katagiri H, and Wasnich RD. Low bone density is not associated with aortic calcification. Calcif Tissue Int. 2001 July. 69(1):20-4.
- 27. Lenchik L, Kiebzak GM, Blunt BA, and the International Society for Clinical Densitometry Position Development Panel and Scientific Advisory Committee. What is the role of serial bone mineral density measurements in patient management? Journal of Clinical Densitometry. 2002. 5(Suppl):S29-S38.
- 28. Lewiecki EM. Management of Osteoporosis. Clin Mol Allergy. 2004 July 14. 2(1):9.
- 29. Lewiecki EM. Vertebroplasty and Kyphoplasty in 2001. J Clin Densitom. 2001. 4(3):185-7.
Last updated on: January 26, 2012
Osteoporosis and Non Specific Chronic Low Back Pain: Correlation with Sex and Severity of Backache
Low Back Pain (LBP) is extremely common-more than 80% of adults have LBP at some time in their life. Usually this is acute (short term) but it can often be chronic, lasting for weeks or even months at a time. Most of the time, the exact cause of the pain cannot be found and this is called as nonspecific LBP. Relationship between OP and nonspecific LBP are not fully clear and the search in this point is limited. Sometimes, chronic LBP may be due to micro fractures resulting from osteoporosis. Compression fractures in the back are a major source of pain and disability for women and some men, over 50 years old. Compression fractures in the back are also the most common type of fracture due to osteoporosis. A vertebral fracture also increases the chance of other future fractures such as a hip fracture. Osteoporosis treatment significantly reduces the chance of future fractures (Palmer et al., 2000).
Osteoporosis is the most common type of metabolic bone disease characterized by low bone mass and micro architectural deterioration. It results either from the bodys inability to form new bone or from an increased resorption of formed bone. Essentially, when there is an imbalance between osteoblastic and osteoclastic activity, skeletal problems may arise. Osteoporosis is a disease of bones that leads to an increased risk of Fracture (Brian et al., 2009). In osteoporosis, the Bone Mineral Density (BMD) is reduced and bone microarchitecture is deteriorated. Osteoporosis by the World Health Organization (WHO) defines as a bone mineral density that is 2.5 (standard deviation) or more below the mean peak bone mass (average of young, healthy adults) are measured by Dual energy X-ray absorptiometry (DEXA); the term “Established osteoporosis”: Include the presence of a fragility Fracture (WHO., 1994). Primary osteoporosis occurs in postmenopausal and secondary osteoporosis may arise at any age and affects men and women equally results from chronic predisposing, medical problems or disease or prolonged use of medications (Old and Calvert, 2004).
Several diagnostic techniques have improved for diagnosis of osteoporosis, most notably Dual-energy X-ray Absorptiometry (DEXA) which is recognized as the reference method to measure bone mineral density (BMD).
The World Health Organization (WHO., 1994) has established DEXA as the best densitometric technique for assessing BMD. DEXA allows accurate diagnosis of osteoporosis, estimation of fracture risk and monitoring of patients undergoing treatment. It can be completed in about 15 min with minimal radiation exposure (about one tenth that of a standard chest x-ray for a quick hips and spine exam).
The WHO define osteoporosis on the basis of the T-score (which is the difference between the measured BMD and the mean value of normal young adults, expressed in Standard Deviations (SD) for a normal population of the same ethnicity) and the diagnostic criteria are, osteoporosis in terms of a T-score below -2.5 and osteopenia when T-score is between -1 and -2.5 (WHO., 1994).
More recently, attention has been focused on deriving measures that provide information about not only bone mineral density but also microstructure. Magnetic resonance imaging (MRI) and Computed Tomography (CT) are such techniques which potentially may provide information pertaining to bone density and structure as well as to occult fracture detection. For example, quantitative CT (QCT), peripheral QCT and quantitative MRI are promising tools for the measurements of the bone density. Micro-CT and magnetic resonance microscopy are potentially available tools to image and quantify the three-dimensional structure of trabecular bone. Magnetic Resonance Imaging (MRI) also has been used to assess risk of fracture (Ishida and Kawai, 2001).
The aim of this study was to evaluate the association of OP with non specific chronic LBP and to evaluate the correlation of OP with sex of the patients and severity of LBP.
MATERIALS AND METHODS
Subjects: The case-control observational study was conducted at Rheumatology and Radiology Departments, Al-Azhar University Hospital, Damietta, Egypt, from February 2013 to October 2014. It comprised 100 adult patients (50 males and 50 females) having non specific chronic LBP for more than 12 weeks. Another 100 healthy subjects (50 males and 50 females) without LBP were employed to act as the control group. The patients and control group were adult subjects of either gender. Informed consent was obtained from all of them. Patients and control groups were selected so that age, body weight and height were matching. All persons having the following inclusion and exclusion criteria.
|•||Age ranged from 20-50 years|
|•||Average height and weight|
|•||All females must be pre-menopausal|
Exclusion criteria: All persons with the following disorders will be excluded from the study:
|•||Endocrinal disease such as diabetes mellitus and hyperthyroidism|
|•||Chronic liver and renal disease|
|•||Smoking and alcoholism|
|•||Collagen diseases as rheumatoid arthritis, systemic lupus and scleroderma|
|•||Known causes of LBP as seronegative spondyloarthropathy, spondylosis, spondylo-litheses, infection, malignancy, disc herniation or prolapse, congenital anomalies and traumas|
Pain Visual Analogue Scale (VAS): To measure LBP intensity for the cases by using a ruler, the score is determined by measuring the distance (mm) on the 10 cm line between the No pain anchor and the patients mark, providing a range of scores from 0-100. A higher score indicates greater pain intensity. Based on the distribution of pain VAS scores, pain intensity classified as none, mild, moderate or severe, the following cut points on the pain VAS have been recommended: No pain (0-4 mm), mild pain (5-44 mm), moderate pain (45-74 mm) and severe pain (75-100 mm) (Aun et al., 1986).
Lumbosacral magnetic resonance imaging (MRI): Using 1.5 tesla Philips closed system), MRI examination was started by explanation of the procedure to the patient to minimize claustrophobia or gross motion. The typical MRI examination were both T1 and T2 weighted images in both axial and sagittal planes. The TI-weighted sequence was performed using TR 400 msec, TE 11I msec, matrix 512×384, slice thickness 4.4 mm, interslice gap 0.4 mm, field of view 325 mm, acquisition time 4 min 24 sec. The T2-weighted sequence was performed using TR 3500 msec, TE 120 msec, matrix 512×384, slice thickness 4.4 mm, interslice gap 0.4 mm, field of view 325 mm, acquisition time 3 min 54 sec. T2 weighting enhances the signal of the cerebrospinal fluid and makes this series more sensitive to spinal disease; the fast spin echo sagittal image was used to assess the central canal and thecal sac compromise by osteophyte or disk. As fat produces an intense signal that can obscure the image, this signal was suppressed by adding a fat-suppression pulse to a spin echo sequence on fatty lesion. The role of MRI in this study to help in exclusion of cases of disc herniation or prolapse, malignancy, infection and to assess the bone density, micro fracture and Shmorls nodules as a signs of osteoporosis.
Dual Energy X-ray Absorptiometry (DEXA): A full table system (capable of multiple skeletal measurements, including the spine and hip) was used. The full table DEXA scanners use a fan-beam source and multiple detectors, the fan beam provides the advantage of decreased scan times compared to single-beam systems. The patient was placed on a table in the path of the radiation beam between the radiation source and detector, the detector placed directly opposite the site to be measured. The source/detector assembly was then scanned across the measurement region. The attenuation of the radiation beam was determined and is related to the Bone Mineral Density (BMD). BMD was the measured parameter and allows the calculation of the Bone Mineral Content (BMC) in grams and the two-dimensional projected area in cm-2 of the bone(s) being measured; thus the units of BMD were g cm-2. The osteoporosis was defined on the basis of the T-score (which is the difference between the measured BMD and the mean value of normal young adults, expressed in Standard Deviations (SD). The T-score was calculated using the formula:
according to the value of T-score the results was as following: Normal BMD when T-score more than -1, osteopenia when T-score was between -1 and -2.4 and osteoporosis when the T-score equal or less than -2.5.
Statistical analysis: The collected data was organized tabulated and statistically analyzed using SPSS (Statistical Package for Social Science) software compute program version 12 (SPSS Inc, USA). The results were represented in tabular forms then interpreted. Mean, standard deviation, range, frequency and percentage were used as descriptive, chi square and Fisher exact test was used for testing significance of observed differences between studied patients. The level of significance was adopted at p<0.05.
Table 1 shows that by DEXA 28 (28.0%) of patients and 15 (15.0%) of control having OP but by MRI, 21 (21.0%) of patients and 10 (10.0%) of control having signs of OP. Figure 1 shows the lumbar spine bone mineral density measures through DEXA Scan while Fig. 2 shows MRI of lumbosacral spine showing Shmorls nodules. As regard DEXA and MRI (Table 2) there are significant difference between patients and control cases (p-value 0.025 and 0.032, respectively).
|Table 1:||Distribution of the cases regarding to DEXA, lumbosacral MRI and VAS|
|Fig. 1:||(DEXA scan): The lumbar spine bone mineral density measures. Based on the WHO, diagnostic categories for osteoporosis, the lowest T score of -2.8 in the lumbar spine indicates osteoporosis|
|Fig. 2:||Lumbosacral spine MRI (T1 and T2) showing Shmorls nodules (Protrusions of the cartilage of the intervertebral disc through the vertebral body endplate and into the adjacent vertebra, due to osteoporosis)|
|Table 2:||Comparison between patients and control groups as regard OP by DEXA and lumbosacral MRI|
|Table 3:||Correlation between OP by DEXA and severity of LBP (VAS)|
|NS**: Non significant|
|Table 4:||Correlation between OP by DEXA with sex of cases|
The results of this study revealed that 28.0% of the cases of non specific LBP had OP by DEXA and 21.0% had signs of OP by MRI and there is significant difference between patients and control cases. There results are in agreement with (Manabe et al., 2003), in a cross-sectional study, who investigated 2,244 women, aged 25-85 years and found that LBP, is associated with lower BMD, concluding that low BMD is an important cause for LBP pain and disabilities. In addition (Snider et al., 2011), studied 63 individuals, 16 of them had LBP and showed that patients with LBP had significantly lower BMD values at the lumbar spine in comparison to the individuals without LBP.
On the other hand and against result of the present study (Atlas and Deyo, 2001), had been reported that low BMD detected by both plain radiographs and advanced imaging studies are poorly associated with LBP.
The present research also revealed that, all the cases (100.0%) that had signs of OP by MRI had also OP by DEXA. But some cases (8.9%) that hadnt signs of OP by MRI, had OP by DEXA. So, DEXA is more sensitive than MRI in diagnosis of OP and it had an advantage for diagnosis of osteopenia than MRI.
This results in agreement with (Balague et al., 2012), that reported that MRI had the advantage of not using ionizing radiation and providing better resolution and provides diagnostic accuracy similar or better than other modalities. However, it has the disadvantage of osteopenia diagnosis.
Putting in mind that, BMD is the most general indicator to diagnose osteoporosis and determine for its treatment and the most important factor to predict osteoporotic fracture. It certainly has weakness that there may be measurement error due to two-dimensional imaging and it cannot reflect bone quality. Yet, it is the most widely used in a clinical setting because the criteria of osteoporosis and osteopenia defined by the WHO are based on BMD (Fujiwara et al., 2003).
Combining advantage and disadvantages of both studied imaging techniques and taking into consideration the higher sensitivity of MRI in relation to DEXA, it is advisable to use DEXA in collaboration with MRI in cases with non specific LBP. When MRI facilities are not available, DEXA alone can be a useful diagnostic tool of OP in cases of LBP.
Also in this study most patients had severe LBP (58.0%) and there was no significant difference between OP and severity of LBP (p-value 0.14 6) and this result in agreement with (Yuan et al., 2011), that reported no evidence for any direct relationship between the two has been found. Although most people believe that OP will lead to LBP, it usually occurs after a vertebral fracture. In contrast one study in Japan (Manabe et al., 2003), showed a positive relationship between BMD and LBP and another study (Makhdoom et al., 2014), concluded that decreased BMD was noticed with increasing severity of chronic back pain.
Risk factors for LBP are poorly understood: the most frequently reported are heavy physical work; frequent bending, twisting, lifting, pulling and pushing; repetitive work; a static posture and vibrations. Psychosocial risk factors include anxiety, depression, job dissatisfaction and mental stress at work. Several risk factors related to inactivity or immobilization was proposed: Reduced muscle strength in the back, abdominal and thigh muscles; reduced endurance in back muscles; hyper mobility of the lumbar column and hypo mobility of hip joints (Hilde and Bo, 1998). Genetics is likely to play a significant role in the development of the processes leading to LBP (Battie et al., 1995). Physical activity (PA) may have dual roles as positive and negative influences on the back (Videman et al., 1995). Prolonged heavy occupational and sports activities seem to increase the risk of LBP but the role of subclinical or more-severe injuries cannot completely be excluded.
Besides physical therapy, many studies suggested vertebroplasty as a treatment of osteoporotic compression fractures. It is a minimally invasive procedure performed to treat both acute and chronic severe back pain associated with vertebral compression fractures. The procedure involves injecting cement into the collapsed vertebral body and can be used to treat a number of underlying causes, including OP, osteonecrosis, painful hemangiomas and malignancies (i.e., pathologic fractures). Most of the published data on vertebroplasty have been favorable (McGirt et al., 2009). Benefits derived from vertebroplasty include pain relief, increased mobility and increased function. Vertebroplasty is indicated in cases of localized pain that impedes function and activities of daily living, where medical treatment either has failed or is contraindicated.
The limitation of this research is due to limited number of the patients because of decrease in the financial supplementation.
OP is usually asymptomatic in the beginning with non-specific symptoms. In later stages, people often suffer from complications from fractures including LBP. Because OA and OP may coexist in aging societies, either high BMD or low BMD may be possible in patients complaining of LBP. The OP is a considerable finding as a cause of non specific LBP, accounting for about 28% of the cases. DEXA is more sensitive than MRI in diagnosis of cases of OP. DEXA alone can be a good diagnostic tool in diagnosis of OP in absence of MRI. No significant difference between OP and severity of backache was observed and most cases of OP were females. It was recommended that every case of non specific chronic LBP to be evaluated by DEXA. More efforts should be extended in getting a thorough history and study.
We are grateful to Professor, Hesham El-Desoky, University of Al Azhar, Faculty of medicine, Damietta, Egypt.