To examine the risk of mortality following all clinical fractures, we followed women age years participating in the Fracture Intervention Trial for an average of 3. All fractures and deaths were confirmed by medical record or death certificate. Clinical fractures were fractures that came to medical attention.
Fracture status was used as a time-dependent covariate in proportional hazards models. They will then carry out a physical examination to reach a diagnosis. Bone healing is a natural process that, in most cases, will occur naturally. Therefore, treatment typically focuses on providing the injured bone with the best circumstances for healing, and ensuring optimal future function.
For the natural healing process to begin, a doctor will reduce the fracture. This involves lining up the ends of the broken bones. In smaller fractures, a doctor can do this by manipulating the affected area externally. However, in some instances, this may require surgery. Once a medical professional has aligned the fracture, they will ensure it stays in place.
Methods of doing so include :. Fractures can take several weeks to several months to heal, depending on their severity. The duration is contingent on which bone has become affected and whether there are any complications, such as a blood supply problem or an infection. Other factors that can affect bone healing include :. After the bone has healed, it may be necessary to restore muscle strength and mobility to the affected area through physical therapy.
If the fracture occurs near or through a joint, there is a risk of permanent stiffness or arthritis. If this happens, a person may not be able to bend that joint as well as before the injury. While bone fractures typically heal well with appropriate treatment, there can be complications, such as:. Non-unions are fractures that fail to heal, while delayed unions are those that take longer to heal. A person can reduce their risk of bone fractures through a number of remedies and lifestyle changes.
The human body needs adequate supplies of calcium for healthy bones. Milk , cheese , yogurt , and dark green leafy vegetables are good sources of calcium. The body also requires vitamin D to absorb calcium. Exposure to sunlight and eating eggs and oily fish are good ways of getting vitamin D. Engaging in weight-bearing exercise can help improve muscle mass and bone density.
Both of these can reduce the risk of bone fractures. Research has shown that regular exercise and a balanced diet can reduce the risk of a fracture in people with osteoporosis. Of the patients, 73 were women and were 27 men. Mean age was 68 years standard deviation: 10 years, range: 50 to 90 years. Demographic data are summarized in Table 1. Five patients had multiple simultaneous fractures and 80 patients had fractures after a fall from standing height. A total of 86 contributors to secondary osteoporosis were diagnosed in 57 patients Table 1 and 2.
Contributors consisted of known medical conditions 34 in 27 patients or newly diagnosed 52 in 50 patients. Seven patients had only known contributors, 20 had known plus a newly diagnosed contributor and 30 had only newly diagnosed contributors. One contributor was found in 32 of whom 24 were vitamin D deficient , more than one contributor in 25 and 43 had none.
Based on serum levels of OHD 3 , 11 patients had severe deficiency, 31 were deficient and 31 had insufficient serum values. All were newly diagnosed. Serum levels of OHD 3 could not be predicted by any of questions on vitamin D or by the sum of those questions. Calcium intake below mg was reported in 86 patients. Calcium intake and serum serum levels of 25OHD3. Only 3 patients had sufficient intake of calcium and normal serum levels of OHD3.
Five patients had secondary hyperparathyroidism, of which four were newly diagnosed Table 2. Hyperparathyroidism was secondary to renal insufficiency in three cases and to low calcium intake in two cases. We found 14 patients with renal insufficiency, of which 6 were newly diagnosed. Three patients were known with hyperthyroidism, 1 new case of exogenous hyperthyroidism and 1 new case of hypothyroidism was detected.
One new case of lactose intolerance was diagnosed. Further contributors included anorexia nervosa in 2 women, documented hypogonadism in one men, pulmonary diseases in 5 patients chronic obstructive lung disease and asthma , alcohol abuse in 4 men, inflammatory rheumatic diseases in 3 patients 2 with rheumatoid arthritis and 1 with giant cell arteritis and 3 with severe immobility.
Most of these patients did not receive preventive measures for osteoporosis prior to the fracture and were thus not recognized as having a contributor to secondary osteoporosis before the fracture occurred.
Among the 9 patients being treated for hypothyroidism, one was over-treated while three were under-treated based on abnormal serum TSH levels. Among the 3 patients being treated for hyperthyroidism, two were under-treated while one was over-treated.
According to the Dutch guideline for osteoporosis 54 patients had clinical bone-related risk factors for fractures in addition to their current fracture Table 4. A history of an additional clinical fracture after the age of 50 was present in 31 patients two with a previous clinical spine fracture. One bone-related risk factor was found in 41 patients, 2 in 12 and 3 in one patient. According to the Dutch guideline for fall prevention, we found fall related risk factors in 79 of the patients: 22 patients had one risk factor, 21 had two risk factors, and 36 had more than two risk factors.
An overlap between clinical bone related risk factors and fall related risk factors was present in 45 patients. VFA could be performed for 93 patients. Lateral spine images were not available in 7 cases due to severe scoliosis or other technical difficulties such as positioning patients with humerus fracture on the DXA table. Prevalence of MVD defined according to the grading of Genant et al.
Based on the FRAX tool, patients with contributors had a higher calculated absolute year risk for major Compared to patients with a high-energy trauma, patients with fragility fractures were older 69 versus 63 years , had better activities of daily living 43 versus 16 patients , and more osteoarthritis 44 versus 4 patients Table 1 and 3.
In the patients older than 50 years presenting with a recent clinical fracture and osteoporosis and referred by the surgeons to the rheumatologists in collaboration with the endocrinologists the prevalence of contributors to secondary osteoporosis was high: almost two out of three patients had one or more contributors most of which were correctable.
The categories of known contributors to secondary osteoporosis were globally similar as reported by Tannennbaum [ 3 ] endocrine, gastrointestinal and inflammatory rheumatic and pulmonary diseases, severe immobility, alcohol abuse. One exception was glucocorticoid users who are presumably frequently referred to an osteoporosis clinic, but were not represented in our group of patients.
Presumably none of the patients with known contributors had received attention in the context of osteoporosis, as none had osteoporosis treatment or calcium and vitamin D supplements. In the other, presumably healthy patients without known contributors, laboratory testing identified newly diagnosed contributors to secondary osteoporosis in 30 more patients, mostly vitamin D deficiency and renal disorders.
In contrast to Tannenbaum, we performed TSH not only in patients with a history of thyroid diseases, but in all patients, and were able to diagnose one new case of hypothyroidism. Vitamin D status could not be identified by history, despite including four specific questions regarding vitamin D intake.
It has been shown that there is only a modest relation between reported vitamin D intake from an extensive dietary questionnaire and serum levels of OHD3 [ 30 ]. In our study a wide spectrum of levels of serum OHD3 were found, from severely deficient to normal. There is still no consensus about how much vitamin D supplements are required to normalise serum levels.
As patients with low serum levels of OHD 3 require, at least temporarily, high doses of vitamin D supplements while those with normal levels require less or none [ 34 ], measuring serum OHD3 levels is helpful in patients with osteoporosis in order to decide about appropriate vitamin D supplementation [ 3 ].
Correcting these combined deficiencies has been demonstrated to reduce fracture risk, at least in institutionalized elderly women [ 35 ] and to reduce the risk of falls [ 36 ]. Calcium and vitamin D supplementation are thus needed in most patients presenting with a fracture and osteoporosis. However, supplementation with calcium and vitamin D alone is an insufficient measure in patients with osteoporosis, as drug therapy for osteoporosis has been shown to reduce the risk of fractures on top of correcting such deficiencies.
Our data, together with those of Edwards et al. Interestingly, the presence of contributors was similar between women and men, and between patients with fractures associated with low or high-energy trauma, suggesting that evaluation for secondary contributors is indicated in women and men and after low or high-energetic trauma.
An additional 14 patients had laboratory abnormalities that required further investigation, mainly hypercalciuria, uncontrolled treatment of thyroid disorders and low testosterone in one man. Hyperthyroidism, whether endogenous or exogenous, can increases bone turnover and contributes to secondary osteoporosis [ 37 , 38 ].
Hypothyroidism on the other hand increases the risk of fractures through low bone turnover if untreated or high bone turnover if over treated [ 39 ]. Thus fine-tuning thyroid treatment is indicated. The same is probably true for patients with hypercalciuria in whom thiazides are indicated [ 40 ], and for hypogonadism in men that can be treated with testosterone supplementation [ 41 ], although no fracture prevention data are available in these conditions. As many patients had endocrine diseases, collaboration with endocrinologists appeared to be highly valuable for diagnosis and treatment.
The prevalence of clinical bone-related fracture risks in postmenopausal women, as evaluated by the Dutch guidelines, was similar between patients with and without documented contributors to and it contributed to further specify the risk for fractures. Although it has not been shown until now that fall prevention strategies itself can prevent fractures, they reduce the risk of falls.
An interesting finding was the prevalence of MVD which was more than twice as high among patients with documented contributors for secondary osteoporosis compared to those without contributors, in spite of similar low BMD in both groups.
MVDs, that are related to future fracture risk independent of BMD [ 11 ], reflect bone failure independently of BMD and thus indicate other mechanisms of bone's decreased resistance to fracture than low BMD, such as changes in the bone turnover, alterations in micro architecture of bone and deficient mineralization, especially in the context of the high prevalence of calcium and vitamin D deficiency.
In several recent publications differential diagnosis and search for contributors to secondary osteoporosis is advocated [ 44 , 45 ]. Only limited data are available about collaboration between surgeons and internists in taking care for osteoporosis in patients presenting with a fracture.
Some initiatives were very successful [ 46 ], but in most instances the collaboration is failing [ 47 ]. This study indicates that such collaborations add to better treatment of patients with a clinical fracture. This study has several limitations. The sample size was relatively small, but the strength of the study was that consecutive patients were evaluated showing that even in a small group many contributors to secondary osteoporosis could be diagnosed. Some laboratory abnormalities needed further exploration, but were not followed up and so no definite diagnosis could be reported in these patients.
VFA has several limitations. Not all vertebrae could be measured, mainly at the upper thoracic level. Identifying patients with MVD by VFA requires additional X-rays to differentiate deformities due to other conditions, such as Scheuerman's disease, degenerative changes or non-osteoporotic short vertebral height.
However, the method has a high negative predictive value in predicting the absence of vertebral fractures on X-rays [ 27 ].
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