An exercise program should include both muscle strengthening and weight bearing exercises. Muscle strengthening exercises may include:.
Weight-bearing exercises include activities, such as dancing, stair climbing, and walking. Tai chi or yoga can help preserve flexibility. Balancing exercises might also help prevent falls as a person gets older, decreasing the risk of breaks. If a person with osteopenia has already suffered a bone fracture, however, doctors may prescribe medication. Medication may include a class of drugs called bisphosphonates that work by preventing bone reabsorption.
For people whose bone density has progresssed to the level of osteoporosis, doctors may prescribe medication, such as hormone replacement therapy HRT. Osteoporosis leaves bones fragile, which can mean that even minor falls may cause bone fractures. It can also lead to stooped posture, loss of height, and a collapsed vertebra.
According to the National Osteoporosis Foundation, about 54 million people in the United States have osteoporosis. Many more people are estimated to have osteopenia. It is important to understand that people with osteopenia are at an increased risk of developing osteoporosis.
Many of the strategies adopted for preventing osteopenia can be applied to treating the condition. For example, regularly participating in weight-bearing exercise can decrease the risk of developing osteopenia. Eating a well-balanced diet including foods high in calcium and vitamin D is also helpful in preventing bone loss.
People who do not get enough calcium and vitamin D in the foods they eat should ask their doctor about supplements. The amount of calcium a person needs may vary based on age, gender, and other underlying risk factors for osteopenia. Osteoporosis occurs when bone density decreases. This affects the structure and strength of bones and makes fractures more likely. Osteoporosis is…. In revised guidelines, the ACP strongly advise that women with osteoporosis should be treated with bisphosphonates or denosumab to prevent bone….
A new study reveals that the protein Cbf-beta switches progenitor cells from creating bone-producing cells to creating fat cells in bone marrow….
Please give me your opinion on the best course of action. Fracture risk is commonly estimated by the FRAX tool www. Getting your FRAX result is a critical number to have to help make an informed decision. You will need the exact results of your bone density. If your risk is not so high that medication is recommended, there are many things you can do to help your bone density. These include adequate dietary calcium, supplemental vitamin D, regular exercise, especially weight-bearing and strengthening exercises, and avoiding smoking and excess alcohol.
A home evaluation to reduce fall risk may be of benefit. If your fracture risk is already higher than the above threshold, medication would normally be prescribed in addition to lifestyle treatments. Antiresorptive treatments, such as alendronate Fosamax or other bisphosphonate drugs, do increase the risk for jawbone damage, and given what your periodontist has recommended, I would avoid not only these drugs but also denosumab Prolia , which works similarly by decreasing bone resorption.
Although I am not an expert, I would consider treatment with a medicine like teriparatide, which has been used as a treatment for people with jaw osteonecrosis. In patients with BMD-based osteoporosis or presenting with a clinical fracture or both, diagnostic evaluation is necessary to exclude secondary osteoporosis. According to the clinical picture and suspicion, other serum measurements such as plasma cortisol, tests for celiac disease and selected other evaluations looking for secondary causes are indicated [ 28 ].
It is generally considered that secondary causes of osteoporosis are more common in men than women. Among secondary causes, hypogonadism resulting from the treatment of breast cancer with aromatase inhibitors use of androgen deprivation therapies in have become an emerging clinical problem [ 29 ]. There is general consensus on the need for specific osteoporosis treatment in patients with spine or hip fractures and low BMD. For other nonvertebral fractures different societies advocate different strategies.
The NOS recommends drug treatment in all postmenopausal women with a history of any fragility fracture [ 12 ], while the NOF advocates performing a dual-energy x-ray absorptiometry DXA on patients after nonvertebral fractures to decide, whether specific osteoporotic therapy is indicated. General changes in life style like smoking cessation, regular exercise and optimization of nutirition should be implemented in all osteopenic patients.
Patient compliance with these measures is, however, poor, and very few prospective data on the anti-fracture efficacy of such measures exist.. Smoking has emerged as a significant risk factor for fracture in many epidemiological studies [ 30 — 32 ], albeit the influence of dose and duration is less well defined. The same holds for exercise [ 33 , 34 ], but exercise can slow down bone loss after menopause and is important for muscular strength and coordination in the elderly [ 32 ]. The impact of poor nutrition on skeletal health is apparent in its most extreme form in anorexia nervosa, where significant improvement of skeletal mass is important without a reversal of caloric intake in these young women [ 35 , 36 ].
In recent years, vitamin D deficiency has emerged as a very important risk factor for osteoporotic fracture, especially at the hip. High turnover bone loss due to secondary hyperparathyroidism due to vitamin D deficiency is considered a major pathogenetic factor in senile osteoporosis [ 37 ].
Vitamin D deficiency is endemic worldwide [ 38 ] and patients with hip fracture generally have the lowest vitamin D levels among all patient groups studied [ 39 , 40 ]. Vitamin D deficiency does not only cause weaker bones due to osteomalacia, but also severe myopathy with loss of muscle strength, selective loss of the rapid type-2 fibres, dyscoordination and consequently increased propensity for falls [ 41 ].
It is therefore not surprising that meta-analyses indicate that correction of vitamin D deficiency results in a decreased fall and fracture risk [ 42 , 43 ], but the effects depend on the dose of vitamin D and the target population [ 44 ]. In a recent controlled clinical trial Bischoff-Ferrari et al. In this context, it is reassuring that, when intake of vitamin D3 is sufficient, the need for calcium intake is considered to be lower [ 49 ].
Vitamin D supplements improve muscle function and decrease the risk of falls, as discussed above. The role of physical exercise is still debated, but exercise interventions together with other measures such as removing loose carpets, reduce use of sleep medicine and other tranquilizers, correct visual impairment etc.
The role of hip protectors remains controversial. They seem to work in nursing homes [ 51 , 52 ], but less in community dwelling elderly, mainly due to discomfort and practicality [ 53 , 54 ]. The last 2 decades have seen the emergence of an ever growing list of effective and safe pharmacological agents for the treatment of osteoporosis. These therapies for the prevention and treatment of osteoporosis affect bone remodeling by either inhibiting bone resorption antiresorptive or anti-activation drugs or enhancing bone formation anabolic regimens.
Antiresorptive drugs do not lead to net accrual of bone in the skeleton, despite the fact that BMD is increased. They mainly act by reducing bone turnover therefore the term anti-activation , thus reducing the impact of the negative remodeling balance present in osteoporotics [ 55 ] and limiting further deterioration of cancellous- and cortical bone structure [ 56 ].
These drugs also reduce the remodeling space and increase the degree by which bone matrix is mineralized, which is behind the increase in BMD and add to the antifracture efficacy of these agents. Antiresorptives belonging to the bisphosphonate group are the most widely used agents. In hip fracture patients, treatment with iv.
Anabolic drugs, of which only recombinant PTH are currently available, on the other hand add net bone mass to the skeleton and actually improve bone structure and increase bone size from the osteoporotic state [ 60 , 61 ]. Estrogen receptors have been demonstrated on both osteoblasts and osteoclasts [ 62 , 63 ]. These results led to less enthusiasm for long-term estrogen therapy world wide.
Current recommendations support restricting the use of estrogen in most women to 5 years in the perimenopausal period [ 67 ], with the aim mainly to reduce hot flushes and other postmenopausal symptoms, and regular mammography should be performed. Selective estrogen receptor modulators SERMs are non-steroidal synthetic agents, which exert estrogen-like properties on the bone and cardiovascular systems, but estrogen antagonistic actions in the breast and, in some cases, the endometrium.
The first SERM developed both for breast cancer prevention and for osteoporosis, raloxifene, is now approved in many countries for the treatment of osteoporosis. In some women hot flashes and other menopausal symptoms may recur on raloxifene. Similar to estrogen, raloxifene, increases the risk of deep venous thrombosis three-fold [ 68 ].
The STAR trial comparing raloxifene to Tamoxifen found reported that Raloxifene was as effective as tamoxifen in reducing the risk of invasive breast cancer and carried a lower risk of thromboembolic events and cataracts, but a non-statistically significant higher risk of non-invasive breast cancer.
The risk of other cancers, fractures, ischemic heart disease, and stroke was similar for both drugs [ 71 ]. The drug caused significant reductions compared with placebo in vertebral and nonvertebral but not hip fracture risk as well as in estrogen receptor positive breast cancer with the 0.
This is the only SERM, to date showing significant reduction of nonvertebral fractures as well as significant reductions in risk of stroke, cholesterol levels and cardiovascular disease [ 72 , 73 ].
In this study, however, a small rise in overall mortality was reported in the 0. In hypogonadal males low testosterone levels result in a high turnover state in bone leading to bone loss and increased risk of fracture.
The main driver of this turnover increase is low circulating estrogen levels, just as in postmenopausal women [ 74 ]. The low estrogen arises from insufficient aromatase conversion from testosterone, either due to low testosterone levels or insufficient aromatase activity [ 75 ].
Testosterone replacement therapy in hypogonadism will increase circulating estradiol levels and thereby reduce bone turnover and increase BMD [ 76 ]. Due to the fear of inducing prostate cancer clinicians have, however, been quite reluctant to institute testosterone replacement therapy.
Recent data suggest, however, that prostate cancers occurring in hypogonadal males have a worse prognosis than cancers occurring in eugonadism,[ 79 ]. Moreover, 16 population studies were unable to demonstrate any relation between testosterone levels and risk kfo prostate cancer [ 80 ].
Nevertheless, regular controls of prostate specific antigen PSA and digitial rectal exploration before and after institution of therapy is still warranted.
Calcitonin has been shown to improve bone structure in the forearm [ 83 ]. Nasal calcitonin is generally well tolerated, with occasional rhinitis. Headache, flushing, nausea, and diarrhoea have been reported more commonly with subcutaneous, than with intranasal calcitonin.
Due to the absence of significant reductions in hip- and nonvertebral fractures calcitonin is considered a second- or third-line agent for osteoporosis treatment in most countries. Bisphosphonates are potent inhibitors of bone resorption and reduce the risk of osteoporotic fractures when administered orally or by intravenous infusion [ 84 ].
They are simple molecules with a P-C-P backbone and variations in the structure of the amino side chains of these drugs determine their pharmacological activity. The most common bisphosphonates licensed and used internationally are alendronate, risedronate, ibandronate, and zoledronic acid. These drugs are used in osteoporosis, Paget disease. In higher doses 10—12 fold the doses used in osteoporosis these drugs are used for the treatment of advanced metastatic cancer with bone involvement e.
This limitation is overcome by iv administration. After absorption the drugs are primarily going to the skeleton or excreted via the kidneys. This results in absence of detectable bisphosphonate in the circulation 2—3 days after administration, while the drugs exhibit a variable but generally long skeletal retention years to tens of years. Once adsorbed onto bone surfaces, the mechanism of action is based on two actions: 1 tight binding to hydroxyapatite crystals in bone; 2 inhibition of important metabolic pathways in osteoclasts after incorporation during resorption of bisphosphonate coated bone.
The latter mechanism is either via accumulation of toxic ATP analogues for non-nitrogen containing bisphosphonates or inhibition of a key enzyme in the mevalonate pathway by nitrogen containing bisphosphonates impairing cholesterol metabolism of the osteoclast and leading to cytoskeletal alterations and premature osteoclast cell death via apoptosis [ 84 ].
Histomorphometric analyses of bone biopsies obtained from patients treated with bisphosphonates have revealed dose dependent reduction in bone turnover, without any adverse effects on osteoblastic function or matrix mineralization [ 85 , 86 ].
A few studies have also demonstrated improved balance at the BMU-level [ 87 ]. Over prolonged administration, continued local inhibition of continuously deposited and recycled bisphosphonates may partially account for a lack of rapid loss of BMD gains, when these agents are discontinued [ 88 ], which is a unique property, compared to other osteoporosis treatments.
The main side effect of oral bisphosphonates is gastrointestinal GI intolerance, [ 89 ]. Most reported GI symptoms have been non-ulcer dyspepsia, but in most clinical trials, no significant differences between those treated with bisphosphonates and those receiving placebo have been demonstrable [ 89 ]. There have been rare reports of severe esophagitis in patients taking oral bisphosphonates [ 90 ]. Recently two purported adverse effects to long term bisphosphonate treatment have been reported and been subject to significant scrutiny: 1 osteonecrosis of the jaw ONJ 2 atypical femoral fractures.
In relation to ONJ it is important to distinguish between patients receiving bisphosphonate therapy for advanced cancer with bone metastases and patients receiving the drug for the treatment of osteoporosis. In oncology only iv. Among malignancies the vast majority of ONJ cases are seen in myeloma and breast cancer.
The underlying cause of this selectivity is still unknown. Cases also have been described in patients receiving bisphosphonates for osteoporosis, but are much rarer.
Atypical femoral fractures have also been reported in several small case series and are mostly transverse fractures of the femoral shaft in patients on long term treatment with alendronate.
The fracture event is usually preceded by longstanding pain in the affected hip and most fractures happen without fall-related trauma. Bilateral fractures may occur, and on x-rays, signs of periosteal reaction and diffuse or focal cortical thickening are usually seen [ 94 ]. Whether direct causality between bisphosphonate use and these fractures can ever be established is doubtful. Currently, the general consensus is that the benefit of significant reduction of all hip fractures after bisphosphonate treatment far outweighs the small risk of an atypical fracture, but strategies are being developed in order to identify individuals at risk.
Alendronate was the first amino-bisphosphonate approved by the US Food and Drug Administration for the treatment and prevention of osteoporosis. With the exception of clinical vertebral fractures, fracture risk reduction at other skeletal sites was statistically indistinguishable in those receiving 5 years on followed by 5 years off of alendronate versus a full 10 years of therapy [ 88 ]. Later, however, once-weekly preparation of alendronate 70 mg has greatly exceeded daily administration based on improved ease of use, and tolerability that is equivalent to or better than daily therapy [ 97 ].
The decision about whether to stop therapy with bisphosphonate after a finite period of time is subject to debate. Risedronate is a pyridinyl amino-bisphosphonate that increases bone mass and prevents fractures [ 99 ]. The drug was also tested In the Hip Intervention Program study, where risedronate 5 mg significantly reduced hip fractures among women with confirmed low bone mass but not among those selected primarily on the basis of fall risks without documented osteoporosis [ ].
The drug was also tested in women and men after surgical repair of a hip fracture, and in this population a significant reduction in subsequent clinical fractures along with a reduction in mortality was seen [ 10 ]. As with other iv. These symptoms are seen mainly after administration of the first dose, but rarely with subsequent dosing, and seem to be less pronounced in patients previously treated with oral bisphosphonates.
Due to the higher Cmax achieved with iv bisphosphonates the risk of renal impairment is increased over oral adminsitration. However, if a minimum infusion time of 15 min is adhered to. The FIT II study studied 8, women with low fermoral neck BMD, but no prevalent vertebral fractures, who were randomized to alendronate 5—10 mg or placebo for a period of 4 years. The primary endpoint was reduction of all clinical fractures spine, hip, nonvertebral [ 8 ]. The NNT to prevent 1 vertebral fracture ranged between 59 and in the lower and higher osteopenic range, respectively [ 8 ].
Continuous excessive secretion of parathyroid hormone PTH e. In contrast, exogenously administered intermittent PTH leading to a peak of excess PTH for about 3 h is anabolic due to stimulation of osteoblastic bone formation and increased skeletal remodeling activity. Daily administration of the approved dose of 20 ug of PTH fragment [ 1 — 34 ] teriparatide increased BMD by an average of 9.
The initial decrease at this site, coincides with the maximal increase in cortical porosity seen with the drug at 6 months [ ]. Teriparatide increases cancellous bone volume, restores trabecular bone architecture and increases cortical thickness.
It also leads to periosteal new bone formation and increases cross-sectional area, potentially increasing cortical bone strength [ ]. Full length PTH [ 1 — 84 ] has also been tested as a treatment modality for osteoporosis.
No reduction of nonvertebral fractures was demonstrable [ ]. Clinical trials of teriparatide were terminated early by the finding of osteosarcoma in Fisher rats [ 61 ], and similar effects were seen with PTH [ 1 — 84 ]. However after widespread use in humans no significant increase in osteosarcoma cases beyond the background rate has been detected. Due to this finding in the initial trial and in repeated toxicology trials in rats, PTH is recommended for treatment for a limited period of months.
There is an enhanced effect on bone mass when PTH is sequentially followed by antiresorptives like alendronate [ ] or estrogen [ ], most probably due to a reduction of the remodeling space brought about by these agents. If some kind of antiresorptive treatment is not given, bone mass will return to baseline within 2 years after discontinuation of PTH, albeit anti-fracture efficacy seems preserved [ ].
Oral bisphosphonates started prior to or concurrently with PTH may attenuate bone mass improvement and bone marker increases seen with PTH alone. Bisphosphonates seem to be causing less blunting of the BMD and marker response [ ]. PTH is currently used most commonly in adults with severe osteoporosis,—many of whom have had fractures while on other antiosteoporotic agents or have had intolerance to bisphosphonates, and will rarely have indications in osteopenic patients.
Denusomab, a specific recombinant humanized monoclonal antibody against RANKL, is the most effective suppressor of bone resorption yet developed. Consequently the BMD increases seen are more pronounced than with other antiresorptives. In clinical trials with Denosumab, overall adverse events were similar to placebo. There was no increase in the risk of cancer, infection, cardiovascular disease, delayed fracture healing, or hypocalcemia.
In the osteoporosis trials with Denosumab there were no cases of osteonecrosis of the jaw. In the oncology trials with Denosumab, however, the risk of ONJ was found to be similar to that of Zoledronic acid [ ].
Daily intake of strontium ranelate has been shown to reduce the risk of vertebral and nonvertebral fractures in postmenopausal women with osteoporosis or a prevalent vertebral fracture or both. Other post hoc analyses have demonstrated efficacy in women with osteopenia and women older than 80 years [ ].
An ever increasing array of effective treatments is at our disposal, to protect patients with osteopenia against fractures. While there is general consensus on treating osteopenic individuals with prevalent low energy fractures, the treatment of osteopenia without fracture is still debatable.
However, current evidence indicates that specific pharmacotherapy should be instituted if an osteopenic patients has prevalent fractures or suffers new fractures, be it clinical or asymptomatic. Moreover, a significant accumulation of several significant risk factors, for example as indicated by the FRAX tool may constitute an indication for pharmacotherapy.
Assessment and intervention thresholds based on the year risk of major fracture, as calculated from FRAX. Amino-bisphosphonates, taken orally or intravenously, remain the dominant treatment modalities for osteoporosis. They reduce fracture risk in osteoporotic as well as osteopenic individuals. Denosumab constitutes a future alternative to bisphosphonates. Similarly SERMs should be considered in younger postmenopausal women, especially those at increased risk of breast cancer.
In males with low testosterone levels, testosterone substitution is indicated as it improves skeletal integrity. We still need long term controlled studies on this treatment, but the risk of prostate cancer does not seem to be as big as previously anticipated.
Teriparatide, would currently rarely be considered in women or men with cheaper anabolics available, however, initial therapy with anabolics to bring osteopenic patients out of the risk zone followed by an antiresorptive would probably be the ideal treatment. This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author s and source are credited.
National Center for Biotechnology Information , U. Rev Endocr Metab Disord. Published online Jun Erik Fink Eriksen. Author information Copyright and License information Disclaimer. Erik Fink Eriksen, Email: on. Corresponding author. This article has been cited by other articles in PMC.
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