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What is Patellar Tendinitis?

What is Patellar Tendinitis?

Patellar tendinitis is a common health issue characterized by the inflammation of the tendon which joins the kneecap, or patella, to the shinbone, or tibia. The knee pain associated with this problem may range from mild to severe depending on the circumstances of the knee injury.

Patellar tendinitis, or jumper’s knee, is a well-known sports injury among athletes who play in basketball and volleyball. Among recreational volleyball players, an estimated 14.4 percent of them have jumper’s knee, where the incidence is even higher for professional athletes. An estimated 40 to 50 percent of elite volleyball players have patellar tendinitis.

Causes of Patellar Tendinitis

Patellar tendinitis is caused by repetitive strain on the knee, most often from overuse in physical activities. Stress can create tears along the tendons which can cause inflammation in the complex structures of the knee.

Other contributing factors of patellar tendinitis include:

  • Tight or stiff leg muscles
  • Uneven leg muscle strength
  • Misaligned toes, ankles, and legs
  • Obesity
  • Sneakers without enough padding
  • Tough playing surfaces
  • Chronic health issues that weaken the tendon

Athletes have a higher chance of developing patellar tendinitis because running, jumping, and squatting put more force over the tendon. Running can place a force of as many as five times the body weight on the knees.

Intense physical activity for an extended amount of time has been previously associated with jumper’s knee. A 2014 research study noted that jump frequency was also a significant risk factor for amateur players.

Symptoms of Patellar Tendinitis

The initial symptoms of patellar tendinitis include pain,�discomfort, and tenderness at the base of the kneecap or patella. Other symptoms of patellar tendinitis may include a burning sensation. For many patients, getting up from a squat or kneeling down can also be particularly debilitating.

The pain associated with patellar tendinitis may be irregular at first, manifesting immediately after participating in physical activities. Damage or injury to the tendon can also make the pain worse. Jumper’s knee can affect regular daily activities, such as climbing stairs or sitting in a vehicle.

Dr Jimenez White Coat

Patellar tendinitis, also known as “jumper’s knee”, is a particularly common cause of pain and discomfort in the patellar region of many athletes. While it frequently occurs as a result of repetitive or continuous jumping, research studies have demonstrated that patellar tendinitis may be associated with stiff ankle movements and ankle sprains, among other sports injuries.

Dr. Alex Jimenez D.C., C.C.S.T. Insight

Patellar Tendinitis Diagnosis

At the start of a�consultation, the healthcare professional will first ask the patient about their specific health issue. The doctor will then physically evaluate the patient’s knee, probe for where they are feeling pain, and test the assortment of knee motion by bending and extending the patient’s leg.

Furthermore, the healthcare professional may additionally order imaging diagnostics to find out if there’s any damage or injury to the tendon or even the bone. These tests can help rule out a broken bone, or fracture. The doctor may use an X-ray to look for a displaced or fractured kneecap, and an MRI or an ultrasound to reveal any harm to the soft tissue.

 

 

Patellar Tendinitis Treatment

Treatment for patellar tendinitis depends on the damage or injury to the knee. Conservative steps to reduce pain, such as rest or exercises are generally the first line of treatment. The healthcare professional will usually recommend a span of controlled rest, where they will prevent the patient from engaging in physical activities that put�pressure on the knee.

Drugs and/or Medications

The healthcare professional may prescribe over-the-counter drugs and/or medications for short-term pain relief and inflammation reduction.

These can consist of:

  • Ibuprofen (Advil)
  • Naproxen sodium (Aleve)
  • cetaminophen (Tylenol)

If the patient’s symptoms are severe, the healthcare professional may recommend the use of corticosteroid injection in the area around the patellar tendon. This treatment is effective in reducing acute pain.

Another method of utilizing corticosteroid for patellar tendinitis is by spreading the medication over the affected knee and use a low electrical charge to push it through the skin, in a process known as iontophoresis.

Chiropractic Care and Physical Therapy

The goal of chiropractic care and physical therapy for patellar tendinitis is to reduce pain and inflammation, among other symptoms, as well as to strengthen the leg and thigh muscles with stretches and exercises.

If the patient’s symptoms are severe, even while resting, the doctor may recommend that you wear a brace and then use crutches to avoid additional damage or injury to the tendon. If the patient has no painful symptoms, then they can start participating in a physical therapy activities.

A rehabilitation program generally consists of:

  • A warm-up interval
  • Massage, heat or ice to the�knee
  • Stretching exercises
  • Strengthening exercises

A doctor of chiropractic, or chiropractor, may use ultrasound and electrical stimulation to relieve the patient’s knee pain. A�knee brace or taping of the knee might also help reduce pain by supporting the kneecap when engaging in physical activities. The healthcare professional may develop a workout program that may include a series of stretches and exercises.

Surgery

When other treatments are not effective in relieving painful symptoms associated with patellar tendinitis, the doctor may advise surgery to repair the patellar tendon. Traditional surgery involves opening the knee to scrape on the kneecap and tendon. More recently,�arthroscopic surgery is used for this particular process. This surgical intervention involves making four small incisions in the knee and it has a shorter recovery time.

The recovery period for surgery varies per procedure. Some surgical intervention advise for immobilization with a cast. Others suggest�an immediate rehabilitation program. Regardless of the level of damage and/or injury, it’s essential for patients to seek medical attention for their patellar tendinitis. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

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Additional Topic Discussion: Relieving Knee Pain without Surgery

Knee pain is a well-known symptom which can occur due to a variety of knee injuries and/or conditions, including sports injuries. The knee is one of the most complex joints in the human body as it is made-up of the intersection of four bones, four ligaments, various tendons, two menisci, and cartilage. According to the American Academy of Family Physicians, the most common causes of knee pain include patellar subluxation, patellar tendinitis or jumper’s knee, and Osgood-Schlatter disease. Although knee pain is most likely to occur in people over 60 years old, knee pain can also occur in children and adolescents. Knee pain can be treated at home following the RICE methods, however, severe knee injuries may require immediate medical attention, including chiropractic care.

 

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EXTRA EXTRA | IMPORTANT TOPIC: Chiropractic Care El Paso, TX Knee Injury

Bisphosphonates: Mechanism of Action and Role in Clinical Practice

Bisphosphonates: Mechanism of Action and Role in Clinical Practice

Bisphosphonates are a type of drug/medication which blocks the loss of bone density to treat osteoporosis-related ailments. They are most frequently prescribed for the treatment of osteoporosis. Bisphosphonates have two phosphonate groups. Evidence demonstrates that they reduce the probability of fractures in post-menopausal women with osteoporosis.

Bone tissue undergoes continuous remodeling that is stored to provide equilibrium, or homeostasis, through osteoblasts generating bone and osteoclasts ruining bone. Bisphosphonates inhibit bone digestion by encouraging osteoclasts to undergo apoptosis or cell death.

The uses of bisphosphonates include the prevention and treatment of osteoporosis, Paget’s disease of bone, bone metastasis (with or without hypercalcaemia), multiple myeloma, primary hyperparathyroidism, osteogenesis imperfecta, fibrous dysplasia, and other conditions which exhibit bone fragility. The purpose of the following article is to discuss the mechanism of action and role in the clinical practice of bisphosphonates.

Abstract

Bisphosphonates are primary agents in the current pharmacological arsenal against osteoclast-mediated bone loss due to osteoporosis, Paget disease of bone, malignancies metastatic to bone, multiple myeloma, and hypercalcemia of malignancy. In addition to currently approved uses, bisphosphonates are commonly prescribed for prevention and treatment of a variety of other skeletal conditions, such as low bone density and osteogenesis imperfecta. However, the recent recognition that bisphosphonate use is associated with pathologic conditions including osteonecrosis of the jaw has sharpened the level of scrutiny of the current widespread use of bisphosphonate therapy. Using the key words bisphosphonate and clinical practice in a PubMed literature search from January 1, 1998, to May 1, 2008, we review current understanding of the mechanisms by which bisphosphonates exert their effects on osteoclasts, discuss the role of bisphosphonates in clinical practice, and highlight some areas of concern associated with bisphosphonate use.

Introduction

Since their introduction to clinical practice more than 3 decades ago, bisphosphonates have been increasingly used for an array of skeletal disorders. Bisphosphonates are now used to treat such varied conditions as heritable skeletal disorders in children, postmenopausal and glucocorticoid-induced osteoporosis (GIO), and bone metastases in patients with malignancies. Bisphosphonates can offer substantial clinical benefit in conditions in which an imbalance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption underlies disease pathology; however, the more recently recognized association of bisphosphonate use with pathologic conditions, including low bone turnover states with resultant pathologic fractures, osteonecrosis of the jaw (ONJ), and an increased incidence of atrial fibrillation, has brought increased scrutiny to the current broad use of bisphosphonate therapy.

PubMed literature from January 1, 1998, to May 1, 2008, was reviewed using bisphosphonate and clinical practice as search terms. Additional articles not obtained in the primary search were identified by assessment of literature referenced in the reviewed articles. We present data on the development of bisphosphonates as therapeutic agents, the proposed mechanisms by which these agents exert their effects, and the current roles for bisphosphonate therapy in clinical practice. Additionally, we address some areas of concern for clinicians and draw attention to some currently unresolved issues associated with bisphosphonate use.

Chemical Structure as Basis for Clinical Activity

Structurally, bisphosphonates are chemically stable derivatives of inorganic pyrophosphate (PPi), a naturally occurring compound in which 2 phosphate groups are linked by esterification (Figure 1, A). Within humans, PPi is released as a by-product of many of the body�s synthetic reactions; thus, it can be readily detected in many tissues, including blood and urine.1 Pioneering studies from the 1960s demonstrated that PPi was capable of inhibiting calcification by binding to hydroxyapatite crystals, leading to the hypothesis that regulation of PPi levels could be the mechanism by which bone mineralization is regulated.2

 

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Like their natural analogue PPi, bisphosphonates have a very high affinity for bone mineral because they bind to hydroxyapatite crystals. Accordingly, bisphosphonate skeletal retention depends on availability of hydroxyapatite binding sites. Bisphosphonates are preferentially incorporated into sites of active bone remodeling, as commonly occurs in conditions characterized by accelerated skeletal turnover. Bisphosphonate not retained in the skeleton is rapidly cleared from the circulation by renal excretion. In addition to their ability to inhibit calcification, bisphosphonates inhibit hydroxyapatite breakdown, thereby effectively suppressing bone resorption.3 This fundamental property of bisphosphonates has led to their utility as clinical agents. More recently, it has been suggested that bisphosphonates also function to limit both osteoblast and osteocyte apoptosis.4,5 The relative importance of this function for bisphosphonate activity is currently unclear.

Modification of the chemical structure of bisphosphonates has widened the differences between the effective bisphosphonate concentrations needed for antiresorptive activity relative to those that inhibit bone matrix mineralization, making the circulating concentrations of all bisphosphonates currently used in clinical practice active essentially only for the inhibition of skeletal resorption.1 As shown in Figure 1, A, the core structure of bisphosphonates differs only slightly from PPi in that bisphosphonates contain a central nonhydrolyzable carbon; the phosphate groups flanking this central carbon are maintained. As detailed in Figure 1, B, and distinct from PPi, nearly all bisphosphonates in current clinical use also have a hydroxyl group attached to the central carbon (termed the R1 position). The flanking phosphate groups provide bisphosphonates with a strong affinity for hydroxyapatite crystals in bone (and are also seen in PPi), whereas the hydroxyl motif further increases a bisphosphonate�s ability to bind calcium. Collectively, the phosphate and hydroxyl groups create a tertiary rather than a binary interaction between the bisphosphonate and the bone matrix, giving bisphosphonates their remarkable specificity for bone.1

Although the phosphate and hydroxyl groups are essential for bisphosphonate affinity for bone matrix, the final structural moiety (in the R2 position) bound to the central carbon is the primary determinant of a bisphosphonate�s potency for inhibition of bone resorption. The presence of a nitrogen or amino group increases the bisphosphonate�s antiresorptive potency by 10 to 10,000 relative to early non�nitrogen-containing bisphosphonates, such as etidronate.1,6 Recent studies (described subsequently) delineate the molecular mechanism by which nitrogen-containing bisphosphonates inhibit osteoclast activity.

A critical pharmacological feature of all bisphosphonates is their extremely high affinity for, and consequent deposition into, bone relative to other tissues. This high affinity for bone mineral allows bisphosphonates to achieve a high local concentration throughout the entire skeleton. Accordingly, bisphosphonates have become the primary therapy for skeletal disorders characterized by excessive or imbalanced skeletal remodeling, in which osteoclast and osteoblast activities are not tightly coupled, leading to excessive osteoclast-mediated bone resorption.

Early non�nitrogen-containing bisphosphonates (etidronate, clodronate, and tiludronate) (Figure 1, B) are considered first-generation bisphosphonates. Because of their close structural similarity to PPi, non�nitrogen-containing bisphosphonates become incorporated into molecules of newly formed adenosine triphosphate (ATP) by the class II aminoacyl�transfer RNA synthetases after osteoclast-mediated uptake from the bone mineral surface.1 Intracellular accumulation of these nonhydrolyzable ATP analogues is believed to be cytotoxic to osteoclasts because they inhibit multiple ATP-dependent cellular processes, leading to osteoclast apoptosis.

Unlike early bisphosphonates, second- and third-generation bisphosphonates (alendronate, risedronate, ibandronate, pamidronate, and zoledronic acid) have nitrogen-containing R2 side chains (Figure 1, C). The mechanism by which nitrogen-containing bisphosphonates promote osteoclast apoptosis is distinct from that of the non�nitrogen-containing bisphosphonates. As elegantly illustrated in recent studies, nitrogen-containing bisphosphonates bind to and inhibit the activity of farnesyl pyrophosphate synthase, a key regulatory enzyme in the mevalonic acid pathway critical to the production of cholesterol, other sterols, and isoprenoid lipids6,7 (Figure 2, A). the analog is likely a direct function of the ability of bisphosphonates to selectively adhere to and be retained within bone before endocytosis within osteoclasts during osteoclast-mediated bone mineral dissolution and matrix digestion (Figure 2, B). Given the fact that nearly all patients now receive treatment with the more potent nitrogen-containing bisphosphonates rather than the earlier non�nitrogen-containing bisphosphonates, the remainder of this review focuses on this more recent class of bisphosphonates.

 

 

Additional Clinical Features

Although bisphosphonate-mediated induction of osteoclast apoptosis cannot be measured directly within the clinical setting, a temporal reduction in biochemical markers of bone resorption (namely amino- and carboxyl-terminal breakdown products of type 1 collagen in serum and urine) after bisphosphonate initiation is considered a reasonably reliable surrogate of bisphosphonate efficacy and potency. Maximum suppression of bone resorption occurs within approximately 3 months of initiation of oral bisphosphonate therapy given daily, weekly, or monthly and remains roughly constant with continuation of treatment.10�12 Resorption is suppressed more rapidly after intravenous (IV) bisphosphonate administration than after oral bisphosphonate therapy.

As might be anticipated, length of suppression is largely a function of bisphosphonate potency for mineral matrix binding, such that the most potent bisphosphonate, zoledronic acid, at a dose of either 4 mg13 or 5 mg (the dose approved by the Food and Drug Administration [FDA] for osteoporosis),14 effectively suppresses biochemical markers of bone resorption for up to 1 year in women with postmenopausal osteoporosis. Although the precise biologic half-lives of the currently used nitrogen-containing bisphosphonates remain the subject of debate largely because of technical challenges required to determine bisphosphonate levels in urine and serum, estimates for the potent bisphosphonate alendronate suggest a biologic half-life of more than 10 years after single-dose IV administration.15

A critical feature governing the clinical pharmacology of bisphosphonates is their bioavailability. As a class, bisphosphonates are very hydrophilic. Accordingly, they are poorly absorbed from the gastrointestinal tract after oral administration (generally with absorption of <1% for an oral dose), instead undergoing paracellular transport because they are not lipophilic.16 Further, only about 50% of the absorbed drug is selectively retained in the skeleton, whereas the remainder is eliminated in the urine without being metabolized. Skeletal uptake and retention are primarily dependent on host factors (renal function, prevalent rate of bone turnover, and binding site availability) and bisphosphonate potency for bone matrix.12 The amount of bisphosphonate retained after either oral or IV administration varies widely both between patients and across clinical conditions and is primarily believed to reflect variations in bone turnover.12

A previous impediment for many patients prescribed oral bisphosphonate therapy was the inconvenience associated with daily oral administration (requiring patients to remain upright for 30 minutes and refrain from eating any food both 2 hours before and at least 30 minutes after pill ingestion) and the relatively common association with gastrointestinal symptoms. The more recent development of pharmacologically equivalent preparations allowing for once-weekly (alendronate or risedronate) or even monthly (ibandronate or risedronate) oral administration has profoundly affected bisphosphonate delivery for most patients for whom convenience (and thus adherence to therapy) was an issue and has correspondingly lead to higher rates of adherence.17,18 Further, the availability of IV preparations (pamidronate, ibandronate, and zoledronic acid), which for most clinical conditions require even less frequent dosing, has eliminated the gastrointestinal adverse effects incurred by some patients managed with oral bisphosphonates, although the rate of acute phase reactions characterized by flulike symptoms (low-grade fever, myalgias and arthralgias, or headache) is increased in patients receiving IV rather than oral bisphosphonate treatment.14

Role in Clinical Practice

As aforementioned, bisphosphonates promote the apoptosis of osteoclasts actively engaged in the degradation of mineral on the bone surface. Accordingly, bisphosphonates have become the primary therapy for managing skeletal conditions characterized by increased osteoclast-mediated bone resorption. Such excessive resorption underlies several pathologic conditions for which bisphosphonates are now commonly used, including multiple forms of osteoporosis (juvenile, postmenopausal or involutional [senile], glucocorticoid-induced, transplant-induced, immobility-induced, and androgen-deprivation�related), Paget disease of bone, osteogenesis imperfecta (OI), hypercalcemia, and malignancy metastatic to bone.

Although each of the nitrogen-containing bisphosphonates is more potent than the non�nitrogen-containing bisphosphonates, their ability to suppress osteoclast activity (as measured by biochemical markers of bone turnover) varies. However, whether superior suppression of bone turnover is relevant for fracture prevention remains to be determined. Indeed, data suggest that adherence to long-term bisphosphonate therapy, rather than the specific bisphosphonate used, is the most important factor in determining the effectiveness of treatment for limiting fracture risk.19,20 Accordingly, studies examining bisphosphonate therapy adherence suggest that, by addressing patient concerns of medication safety and timing, clinicians can significantly improve adherence.21 Whether weekly or monthly oral bisphosphonate dosing leads to higher rates of adherence to therapy is currently unknown.

Osteoporosis

The most common clinical condition for which bisphosphonate therapy is used is osteoporosis, a skeletal condition characterized by compromised bone strength resulting in an increased risk of fracture. As previously noted, osteoporosis is a clinically heterogeneous disease with a range of origins, including hormone loss (postmenopausal and androgen-deprivation), iatrogenic (glucocorticoid-induced and transplant-related), physical (immobility), and genetic (eg, juvenile and OI-associated). Often these conditions overlap within individual patients.

Postmenopausal osteoporosis is characterized by an imbalance between osteoclast-mediated bone resorption and osteoblast-mediated bone formation such that bone resorption is increased. This relative imbalance leads to diminution of skeletal mass, deterioration of bone microarchitecture, and increased fracture risk. During the past 2 decades, bisphosphonate therapy has become the leading clinical intervention for postmenopausal osteoporosis because of the ability of bisphosphonates to selectively suppress osteoclast activity and thereby retard bone resorption. The fracture reduction and concomitant increases in bone density generally seen with bisphosphonate use are believed to result from a decline in the activation frequency of new remodeling units formed by osteoclasts, with relative preservation (at least initially) of osteoblast activity. As such, the initial stabilization and retention of trabecular connectivity allow the duration of secondary mineral deposition on the structural scaffold to be prolonged, thereby increasing the percentage of bone structural units that reach a maximum degree of mineralization.22 This increase in the mean degree of skeletal mineralization underlies both improvements in bone density and reductions in fracture risk after bisphosphonate therapy.

Importantly, this role for bisphosphonates was indirectly buttressed by the early termination of the estrogen and progesterone arm of the Women�s Health Initiative (WHI), because of concern about increased rates of coronary artery disease and breast cancer among women receiving hormonal therapy. For most practitioners and patients, the WHI results effectively limited the practice of treating postmenopausal osteoporosis with hormone replacement therapy, despite the strong evidence provided in the WHI and previous studies that estrogen is highly effective in preventing fractures.23

Among the oral bisphosphonates, both alendronate and risedronate have been conclusively demonstrated to reduce the number of vertebral24�26 and hip fractures,24,27 progression of vertebral deformities, and height loss in postmenopausal women with osteoporosis.28 Ibandronate, developed more recently and available in both oral and IV preparations, has been demonstrated to reduce only the risk of vertebral fracture,29,30 although the sample size estimates used did not allow sufficient power to detect an effect on nonvertebral or hip fractures. The relative fracture risk reduction in vertebral, hip, and nonvertebral sites in post-menopausal women with known osteoporosis after 3 years of bisphosphonate treatment is compared in the Table.

 

 

Reductions in fracture incidence occur before demonstrable changes (measured by dual-energy x-ray absorptiometry [DXA]) in bone mineral density (BMD), suggesting that stabilization of existing skeletal microarchitecture or decreased bone turnover is sufficient for fracture risk reduction.31 Daily alendronate use at doses of 10 mg for up to 10 years was well tolerated and was not associated with adverse skeletal outcomes.32 Whereas nearly all osteoporosis trials in which bisphosphonate therapy has been used involved postmenopausal women, general trials that have examined men with a diagnosis of either low bone mass or osteoporosis have demonstrated similar responses to bisphosphonate therapy.33�35

In the Fracture Intervention Trial Long-term Extension, postmenopausal women with low femoral neck BMD (but not necessarily with DXA-defined osteoporosis) were treated with daily alendronate for 5 years and then randomized to receive either alendronate or placebo for an additional 5 years. Women who discontinued alendronate therapy had statistically significant, although clinically relatively small, declines in BMD and associated increases in biochemical markers of bone turnover compared with women who continued therapy.36 Importantly, no significant differences were found for either nonvertebral fractures or all clinical fractures; however, there was a slightly higher (and statistically significant) risk of clinical vertebral fractures in the placebo group (absolute risk, 2.9%), but this was not a primary or secondary study end point. Formal studies of alendronate cessation with more statistical power for fracture assessment after discontinuation as a primary end point or of other bisphosphonates have not yet established that, for at least some patients with postmenopausal osteoporosis, a drug holiday could be reasonable after a period of bisphosphonate therapy.

Initial studies used daily bisphosphonate dosing; more recent studies have focused on weekly (alendronate and risedronate) or monthly (ibandronate, and more recently risedronate37) dosing, regimens believed to have pharmacodynamic equivalence to daily dosing of each drug. However, all studies to date using intermittent weekly or monthly oral bisphosphonate therapy have relied on surrogate markers, such as biochemical markers of bone resorption or changes in BMD measured by DXA, rather than primary fracture outcomes, for determination of efficacy. In contrast, the BONE trial, in which oral ibandronate was administered every other day for 12 doses every 3 months, did reduce vertebral fractures with intermittent dosing,30 although this dosing regimen is not approved by the FDA for treatment of postmenopausal osteoporosis. Nonetheless, intermittent weekly or monthly therapy is believed to be biologically equivalent for fracture prevention and has become the standard of care.

More recently, both ibandronate and zoledronic acid have been approved for IV administration to treat postmenopausal osteoporosis. Whereas ibandronate is approved for quarterly administration, zoledronic acid is approved for once-yearly administration. During the 3-year Health Outcomes and Reduced Incidence with Zoledronic Acid Once Yearly (HORIZON) study period, annual IV administration of zoledronic acid led to significant decreases in vertebral (70% reduction), hip (41% reduction), and nonvertebral (25% reduction) fractures, with significant increases in BMD at the lumbar spine, hip, and femoral neck.14 In addition, administration of IV zoledronic acid within 90 days of surgical hip fracture repair and yearly thereafter was recently shown to reduce the incidence of any new clinical fracture by 35% and was associated with a 28% reduction in mortality.38 Further, in patients who have been treated with weekly alendronate for at least 1 year, switching to yearly zoledronic acid was not inferior to alendronate continuation, but yearly administration was preferred by patients.39 Whether IV preparations will become preferred bisphosphonate formulations for management of postmenopausal osteoporosis or after hip fracture is unknown. Nonetheless, it is clear that IV bisphosphonate delivery is particularly useful if adherence or gastrointestinal tolerance is a barrier to oral therapy or if patients prefer the relative convenience of IV bisphosphonate therapy.

Finally, several studies have focused on optimal timing of bisphosphonate therapy for management of osteoporosis in conjunction with other pharmacological agents with skeletal activity. Although combining a bisphosphonate with either estrogen or the selective estrogen-receptor modulator raloxifene leads to a slightly greater increase in BMD than treatment with a bisphosphonate alone, no good clinical trial data on fracture rates support routine use of these combinations.40,41 Other studies have evaluated patients receiving either recombinant full-length 1�84 human parathyroid hormone (PTH) or the PTH fragment 1�34 (teriparatide).42�44 In general, prior bisphosphonate treatment appears to blunt the PTH-induced anabolic skeletal response, as does concomitant treatment using bisphosphonate and either PTH or teriparatide.45,46 The most robust skeletal anabolic effects are seen in patients who receive initial PTH treatment and are subsequently maintained with bisphosphonate therapy.35,47,48

Glucocorticoid-Induced and Transplant-Associated Osteoporosis

Whereas bisphosphonates have become the primary therapeutic choice for treatment of postmenopausal osteoporosis, few recognize that glucocorticoid therapy leads to bone loss. A recent study found that most patients receiving long-term glucocorticoid therapy received neither regular BMD assessment nor a prescription for any medication for osteoporosis management.49 Numerous clinical trials have now determined that bisphosphonates are highly effective at limiting bone losses in patients receiving glucocorticoids or transplants. Recent work has shown that, in patients receiving a daily dose of at least 7.5 mg of prednisone, alendronate prevented bone loss more effectively than did the vitamin D3 analogue alfacalcidol.50 Further, in glucocorticoid-treated patients at high risk of fracture, including those with a history of fractures, those with rheumatoid arthritis, or those receiving high doses of glucocorticoid, bisphosphonate therapy is cost-effective.51

Accordingly, risedronate has been approved in the United States for both prevention and treatment of GIO and alendronate for the treatment of GIO. Both are more effective when calcium intake and vitamin D intake are adequate. As well, IV treatment with either pamidronate or ibandronate has been shown to limit skeletal loss from glucocorticoid therapy,52,53 although neither is yet approved for this indication. Notably, multiple studies have documented that both oral and IV bisphosphonate therapy are capable of limiting the bone loss that frequently occurs with either solid organ54�58 or bone marrow transplant.59�62

Finally, a recent study showed that patients with GIO treated with teriparatide had a greater increase in lumbar spine BMD and fewer new vertebral fractures than did patients who received daily alendronate during the course of 18 months.63 Whether teriparatide should supplant bisphosphonate therapy as the treatment of choice for patients with established osteoporosis who are receiving long-term glucocorticoid therapy remains unknown.

Immobility-Induced Osteoporosis and Other Causes of Acute Bone Loss

Immobilized patients, such as those with a recent spinal cord injury or cerebrovascular event, undergo rapid loss of bone, leading to a substantially increased risk of fracture, hypercalcemia, and frequently nephrolithiasis. Both oral (alendronate)64 and IV (pamidronate)65 bisphosphonate therapy have been shown to attenuate this bone loss and reduce biochemical markers of bone resorption. However, the number of clinical trials conducted using both these drugs remains small. Thus, fracture incidence, rates of nephrolithiasis, and long-term safety remain to be determined.

Unlike the generalized bone loss that occurs after immobilization, acute localized periprosthetic bone loss with associated implant loosening is a frequent complication in patients who undergo cementless total hip arthroplasty. Both alendronate66 and risedronate67 attenuate this acute periprosthetic bone loss of the proximal femur, although the long-term effect of bisphosphonate treatment on maintenance of implant integrity has not yet been reported.

Paget Disease of Bone

Whereas postmenopausal osteoporosis is characterized by generalized bone loss from increased osteoclast activity, Paget disease of bone involves 1 or more areas of disordered bone remodeling, in which accelerated osteoclast-mediated bone resorption is followed by imperfect osteoblast-mediated bone deposition.68 The resulting mix of poorly formed woven and lamellar bone frequently results in pain, fractures, and serious deformity, including bowing of weight-bearing long bones, skull enlargement, or numerous other skeletal deformities. As the cornerstone of therapy for Paget disease of bone, bisphosphonates profoundly suppress the increased bone resorption underlying the disease, generally leading to normalization of serum alkaline phosphatase levels used to monitor disease activity. Oral (alendronate69 and risedronate70) and IV (pamidronate71 and the recently approved zoledronic acid72) bisphosphonates are all FDA-approved for the treatment of Paget disease of bone and have largely replaced earlier FDA-approved therapies (non�nitrogen-containing bisphosphonates and calcitonin) because their ability to suppress osteoclast activity is superior.

Bisphosphonates in Malignancy

Many cancers are osteotropic and either metastasize to the skeleton (including but not limited to primary malignancies of the breast, prostate, lung, or kidney) or grow primarily within the bone marrow (multiple myeloma), where this growth frequently leads to hypercalcemia, severe bone pain, skeletal destruction, and pathologic fractures. Indeed, the skeleton is the most common site of metastatic disease, and 90% or more of patients with advanced cancer develop skeletal lesions.73

Breast Cancer

For patients with breast cancer metastatic to bone, treatment with IV preparations of pamidronate,74�76 zoledronic acid,77,78 and ibandronate79 has been shown to substantially relieve skeletal pain and reduce skeletal complications. Of the oral nitrogen-containing bisphosphonates, only ibandronate (given in a daily dosage of 50 mg) has been effective in reducing bone pain and limiting skeletal complications of breast cancer.80,81

Whether bisphosphonate use has an adjunct role in the treatment of women with breast cancer but no evidence of skeletal metastases is currently unknown but is suggested by the provocative finding that women with clinically limited operable breast cancer who received clodronate for 2 years had statistically significant reductions in development of bone metastases while receiving bisphosphonate therapy, as well as reductions in overall mortality when they were followed up for 6 years.82 Although bisphosphonate therapy for women receiving hormonal treatment of breast cancer has received less attention, the important role of limiting bone turnover to maintain skeletal integrity (particularly among premenopausal women in whom pharmacological estrogen deficiency has been introduced) has been more recently appreciated.83 Optimal bisphosphonate management strategies corresponding to numerous available pharmacological ovarian ablation regimens remain to be determined, although zoledronic acid (4 mg IV given every 6 months)84 has recently been demonstrated to prevent bone loss in premenopausal women receiving endocrine-based therapy for hormone-sensitive breast cancer. Likewise, in postmenopausal women with early hormone-dependent breast cancer, weekly oral risedronate was recently shown to prevent bone loss in those receiving aromatase inhibitor therapy.85

Prostate Cancer

Breast cancer is characterized by osteolytic lesions, but skeletal metastases from prostate cancer have been described as osteoblastic. The role of increased bone resorption in metastatic prostate cancer has recently been recognized.86 Among the bisphosphonates, only zoledronic acid has been demonstrated to reduce skeletal bone�related events in men with hormone-refractory prostate cancer,87,88 with an absolute risk reduction of 11% at 2 years compared with placebo.

As with women who undergo chemical hormonal ablation, men with hormone-responsive prostate cancer who receive androgen-deprivation therapy can benefit from judicious bisphosphonate use. Whereas IV pamidronate therapy prevented bone loss at both the hip and the spine in men with nonmetastatic prostate cancer who received gonadotropin-releasing hormone agonist therapy,89 a single annual dose of IV zoledronic acid was recently demonstrated to lead to increases in both spine and hip BMD (rather than the declines seen in patients who received placebo). These results demonstrate that annual IV bisphosphonate treatment can be a useful adjunct to maintain skeletal integrity in androgen-deprived men90 and are similar to results obtained with a more frequent dosing schedule.91 Oral risedronate at a daily dosage of 2.5 mg has also recently been shown to prevent BMD loss at the hip and been associated with a 4.9% increase at the lumbar spine.92

Multiple Myeloma

In multiple myeloma, clonal proliferation of malignant plasma cells within the bone marrow cavity results in osteolysis and skeletal destruction, accounting for much of the morbidity associated with the disease. Multiple studies have shown that both pamidronate and zoledronic acid have an important palliative role in reducing the incidence of hypercalcemia and skeletal bone�related events associated with myeloma,93�95 putting IV bisphosphonates at the center of current therapies to prevent and treat myeloma-associated bone disease. At present, no data support bisphosphonate therapy for patients with smoldering myeloma, myeloma without associated bone disease, or monoclonal gammopathy of undetermined significance, nor is oral bisphosphonate therapy recommended for management of myeloma-associated skeletal disease.

Given that patients with multiple myeloma have the highest incidence of ONJ among all oncology patients receiving bisphosphonate therapy, the choice of bisphosphonate, dosage, and duration of therapy have been the focus of considerable debate, cumulating in clinical practice guidelines from the American Society of Clinical Oncology96 and, more recently, a consensus statement from the Mayo Clinic Myeloma Group97 on the basis of a comprehensive review of the evolving literature. In the Mayo consensus statement, monthly infusion of pamidronate (because of a perceived higher risk of ONJ in patients receiving zoledronic acid) was favored, with discontinuation after 2 years if patients achieve remission and require no further myeloma treatment. If active treatment is still required, pamidronate can be continued at a reduced schedule of every 3 months. Although the International Myeloma Working Group generally agreed with the Mayo consensus statement, the group suggested that pamidronate therapy could be discontinued after a patient is in 1 year of clinical remission and that a reduced dosing schedule was not indicated.98 Thus, although bisphosphonates remain an important aspect of the pharmacological approach to myeloma bone disease, questions regarding their optimal use remain.

Other Malignancies

Use of bisphosphonates in other malignancies less frequently metastatic to bone, such as renal cell carcinoma, has been demonstrated to delay the onset and progression of skeletal disease,99 suggesting that patients with clinical conditions less commonly believed to affect the skeleton can also benefit from bisphosphonate therapy. At present, however, limited data support routine use of bisphosphonate therapy for other malignancies.

Bisphosphonate Therapy for Children

Although bisphosphonates have been used most extensively in adults, during the past decade they have become the mainstay of therapy for OI, a heritable skeletal disorder characterized by substantially diminished bone mass and severe fragility, usually resulting from mutations in the genes for type I collagen. A regimen developed by Glorieux100 of cyclic IV pamidronate (given in 3-day cycles every 2 to 4 months at an annual dose of 9 mg/kg) has been used most successfully, leading to an 88% increase in cortical thickness, a 46% increase in trabecular bone volume,101 and substantial improvement in functional status. More recently, several studies have demonstrated that oral alendronate can also lead to substantial increases in BMD and can limit fractures in OI affecting children.102�104 Although the precise mechanism by which bisphosphonates limit fractures in OI is unknown, histomorphometric analyses of bone biopsy specimens from patients with OI demonstrate increased rates of bone turnover resulting from increased osteoclast relative to osteoblast activity, leading to an overall loss of bone with each remodeling cycle.105 By specifically inhibiting osteoclast-mediated bone resorption, bisphosphonates presumptively allow bone-forming osteoblasts more time to promote bone formation, albeit in the setting of abnormal collagen matrix. Indeed, histomorphometric analyses of iliac crest biopsy specimens from patients with OI who had received pamidronate therapy demonstrated increased cortical thickness and number of trabeculae but no increase in trabecular thickness.101,106

Although bisphosphonate treatment is well established for OI in children, data are limited on efficacy and on risk of harm when bisphosphonates are used in children with osteoporosis secondary to chronic illness (such as cystic fibrosis, juvenile rheumatoid arthritis, or anorexia nervosa) or in those who have had serious burns. A recent systematic review of bisphosphonate therapy for children and adolescents with secondary osteoporosis concluded that too little evidence is available to support bisphosphonates as standard therapy, although treatment for periods of 3 years or less appears to be well tolerated.107 Well-constructed studies are required to develop clear guidelines to diagnose and treat all forms of osteoporosis in children.108

Finally, given the long skeletal half-life of bisphosphonates and evidence that pamidronate can be found in urine specimens up to 8 years after administration,109 care is warranted when considering bisphosphonate treatment for either adolescent or young girls who will reach reproductive maturity within a decade of treatment. At present, only limited, anecdotal data have assessed the safety of long-term pamidronate110 or other bisphosphonate treatment during fetal development.

Dr Jimenez White Coat

Bisphosphonates in clinical practice are utilized to treat osteoporosis, Paget’s disease of the bone, bone metastasis, multiple myeloma, and other health issues with fragile bones. Although bisphosphonates are recommended as one of the first-line treatments for post-menopausal osteoporosis, research studies have previously discussed the adverse effects of this class of drug/medication. It’s essential for patients to talk to their healthcare professional regarding the treatment options for their injuries and/or conditions.

Dr. Alex Jimenez D.C., C.C.S.T. Insight

Clinical Concerns Associated with Bisphosphonate Therapy

Osteonecrosis of the Jaw

Among potential adverse clinical events associated with the use of bisphosphonates, none has received greater attention than ONJ. As reviewed by Woo et al,111 nearly all ONJ cases (94%) have been described in patients receiving high doses of IV bisphosphonates (primarily zoledronic acid and pamidronate) for oncologic conditions. Prevalence in patients with myeloma ranged from 7% to 10%, whereas up to 4% of patients with breast cancer developed ONJ.111,112 More recently, however, a reduced dosing schedule in patients with myeloma, in which IV bisphosphonate was given monthly for 1 year and then every 3 months thereafter, was shown to decrease the incidence of ONJ compared with monthly bisphosphonate infusions.113

Whereas the incidence of ONJ is estimated to be 1 to 10 per 100 oncology patients, the risk of ONJ appears to be substantially lower among patients receiving oral bisphosphonate therapy for osteoporosis, with an estimated incidence of approximately 1 in 10,000 to 1 in 100,000 patient treatment years, although this estimate is based on incomplete data.114 Associated risk factors appear to be poor oral hygiene, a history of dental procedures or denture use, and prolonged exposure to high IV bisphosphonate doses.115,116 Whether concomitant chemotherapy or glucocorticoid use leads to an increased risk of ONJ is unknown.117 Once established, care for ONJ is largely supportive, with antiseptic oral rinses, antibiotics, and limited surgical debridement as necessary leading to healing in most cases.118 Although evidence-based guidelines at this time have not been established for any single malignancy or bisphosphonate, careful attention to dental hygiene including an oral cavity examination for active or anticipated dental issues, both before bisphosphonate initiation and throughout treatment, is likely to be paramount.

Although use of bisphosphonates and development of ONJ have been temporally associated, a causal relationship has not been identified. Thus, despite the burgeoning scientific literature that has developed since the association between bisphosphonate therapy and ONJ was first reported in 2003,119 many fundamental questions remain unanswered. As a first step in this process, a task force convened by the American Society for Bone and Mineral Research recently provided a standardized definition of ONJ as the presence of exposed bone in the maxillofacial region that does not heal within 8 weeks after identification by a health care professional.114 Given the current paucity of information on the true incidence, risk factors, and clinical approach to both prevention and treatment, preclinical basic and animal studies, as well as well-designed clinical trials, are necessary to both identify patients at increased risk of development of ONJ and more fully understand the association between bisphosphonate therapy and ONJ.

Atrial Fibrillation

In addition to the concern for ONJ, another concern with bisphosphonate therapy, which has recently come to light, is atrial fibrillation. In the HORIZON Pivotal Fracture Trial, in which patients were treated annually with IV zoledronic acid, a statistically significant increase in the incidence of serious atrial fibrillation (defined as events resulting in hospitalization or disability or judged to be life-threatening) was noted.14 The etiology of this electrophysiologic abnormality is unknown. Whether other bisphosphonate preparations are associated with increased rates of atrial fibrillation is currently unknown, but recent post hoc analysis of data from the pivotal Fracture Intervention Trials120 and from a large population-based case-control study121 suggest a correlation between alendronate administration and a slightly increased incidence of atrial fibrillation, although a larger population-based case-control study showed no evidence of an increased risk of atrial fibrillation or flutter with alendronate use.122 To date, concerns for atrial fibrillation do not appear to extend to patients receiving risedronate,123 nor was an increased rate of atrial fibrillation seen in the HORIZON Recurrent Fracture Trial, in which patients received IV zoledronic acid after a hip fracture.38 Clearly, more studies examining the potential relationship between bisphosphonate use and atrial fibrillation are warranted, as are focused discussions between clinicians and patients either currently managed with or considering initiation of bisphosphonate treatment.

Oversuppression of Bone Turnover

Because bisphosphonates inhibit osteoclast activity, there has been some concern that prolonged bisphosphonate treatment leads to �frozen bone,� characterized by over-suppression of bone remodeling, an impaired ability to repair skeletal microfractures, and increased skeletal fragility. Although increased rates of microfractures have been found in dogs treated with high doses of bisphosphonates,124 this finding does not appear to be common among postmenopausal women with osteoporosis treated with either oral or IV bisphosphonate therapy,22,125 although isolated cases of severely suppressed bone turnover and associated fractures have been reported.126,127 Nonetheless, the optimal duration of bisphosphonate therapy for postmenopausal osteoporosis, and nearly all other conditions for which bisphosphonates are used, remains unclear.

Hypocalcemia

Hypocalcemia after bisphosphonate administration most frequently follows IV infusion and can occur in patients with high rates of osteoclast-mediated bone resorption (such as in patients with either Paget disease of bone128 or a substantial skeletal tumor burden129), previously unrecognized hypoparathyroidism,130 impaired renal function, or hypovitaminosis D before treatment.131 Treatment is largely supportive, with calcium and vitamin D supplements as appropriate.

Acute Inflammatory Response

Approximately 10% to 30% of patients receiving their first nitrogen-containing bisphosphonate infusion will experience an acute phase reaction, most commonly characterized by transient pyrexia with associated myalgias, arthralgias, headaches, and influenza-like symptoms. This rate declines by more than half with each subsequent infusion, such that a rate of 2.8% was found after the third infusion in the HORIZON trial.14 The acute phase response is believed to be the result of proinflammatory cytokine production by peripheral blood ?? T cells.132 Pretreatment with histamine receptor antagonists or antipyretics can reduce the incidence and severity of symptoms among susceptible patients. Occasionally corticosteroids are of benefit.

A relatively rare adverse effect of bisphosphonate therapy of which physicians should be aware is ocular inflammation (conjunctivitis, uveitis, episcleritis, and scleritis). This complication has been found to occur with both oral and IV bisphosphonate therapy. In the largest retrospective study to date, an incidence of approximately 0.1% was found in patients treated with oral risedronate.133 Fortunately, ocular symptoms usually resolve within a few weeks after bisphosphonate discontinuation.

Severe Musculoskeletal Pain

Although all oral and IV bisphosphonate preparations list musculoskeletal pain as a potential adverse effect in their prescribing information, the US FDA recently issued an alert highlighting the possibility of severe, incapacitating musculoskeletal pain that can occur at any point after initiation of bisphosphonate therapy.134 This severe musculoskeletal pain was distinct from the acute phase response described previously. Fewer than 120 cases had been reported by late 2002 for alendronate and mid-2003 for risedronate in total.135 At this time, both risk factors for and incidence of this adverse effect are unknown.

Other Potential Complications of Bisphosphonate Therapy

Other complications associated with the use of oral and IV bisphosphonate therapies are well recognized. Esophageal irritation and erosion can occur with oral bisphosphonate therapy, particularly in patients with known gastroesophageal reflux disease or esophageal stricture. Strict maintenance of an upright posture for 30 to 60 minutes after ingestion with a full glass of water, depending on the oral bisphosphonate, and the use of weekly rather than daily preparations are both likely to limit the risk of adverse effects. For patients unable to tolerate oral bisphosphonates, IV preparations (as noted previously) are now FDA approved and not associated with gastroesophageal irritation.

Bisphosphonate doses and infusion rates should be adjusted for patients with moderate to severe renal insufficiency. If used in patients with creatine clearance values lower than 30 mL/min, bisphosphonates must be used cautiously. Particularly in patients who receive IV preparations, bisphosphonates can lead to rapid deterioration of renal function,136,137 likely because of their local accumulation in the kidney. For patients with renal insufficiency who receive IV bisphosphonate therapy, renal function both before and after drug administration should be determined. In patients with mild to moderate renal impairment, oral bisphosphonates rarely lead to further deterioration in renal function, likely because of their poor absorption across the gastrointestinal tract and thus limited short-term bioavailability.

Unresolved Questions

Bisphosphonates have been and continue to be used for other conditions without an FDA-approved indication for therapy. As noted, these include various pediatric populations with low bone mass, incident fractures, and prolonged immobility. Many healthy premenopausal women with either radiographic osteopenia or osteoporosis without fractures and postmenopausal women with osteopenia but without fractures now receive bisphosphonate therapy. Until further studies address these important clinical questions, it is important to tell such patients that we currently lack sufficient data from well-controlled clinical trials to determine either benefits or risks assumed with these pharmacological interventions.

Role of Calcium and Vitamin D

Despite the good intentions of many practitioners to limit fractures in their patients by instituting bisphosphonate therapy, the importance of assuring adequate vitamin D and calcium intake both before and after starting bisphosphate therapy is frequently overlooked. Hypovitaminosis D is common among many patient populations that are also prescribed bisphosphonate therapy and is particularly common among elderly patients who frequently have limited sun exposure, reduced dietary intake, or some renal impairment. This vitamin D insufficiency or deficiency limits dietary absorption of calcium, leading to secondary hyperparathyroidism and loss of skeletal calcium to maintain normocalcemia. Accordingly, among elderly women with osteoporosis, the persistence of secondary hyperparathyroidism blunted the increase in BMD in the lumbar spine in response to weekly alendronate.138 Although currently available data offer no consensus on optimal serum levels of 25-hydroxyvitamin D, a level of 30 ng/mL (75 nmol/L) or more is generally considered to be adequate; vitamin D intoxication occurs only when levels are higher than 150 ng/mL (374 nmol/L).139 For a more complete review of the role of vitamin D in maintenance of skeletal health and for recommendations for vitamin D replacement, please refer to the excellent recent review by Holick.139

Although guidelines for the maintenance of optimal vitamin D levels have changed substantially as we appreciate that vitamin D insufficiency and deficiency affect a far greater proportion of the population than previously recognized, recommendations for optimal calcium intake have been modified only slightly since being addressed by an expert panel convened by the National Institutes of Health in 1994.140 The panel concluded that optimal calcium intake is estimated to be 1000 mg/d for both premenopausal and postmenopausal women receiving estrogen replacement therapy and 1500 mg/d for postmenopausal women not receiving estrogen. Men younger than 65 years were estimated to require 1000 mg/d of calcium and men older than 65 years to require 1500 mg/d.140 More recent recommendations from the National Osteoporosis Foundation have suggested a calcium intake of 1000 mg/d for both men and women younger than 50 years, with an increase to 1200 mg/d from age 50 years onward.141 These recommendations are consistent with those of the Food and Nutrition Board of the Institute of Medicine.142 Further recommendations for calcium intake in children are detailed in both the National Institutes of Health�s and Institute of Medicine�s guidelines.140,142

Conclusion

Since their introduction to clinical practice, bisphosphonates have transformed the clinical care of an array of skeletal disorders characterized by excessive osteoclast-mediated bone resorption. Accordingly, the informed and judicious use of bisphosphonates confers a clear clinical benefit for carefully selected patients that outweighs the risks associated with bisphosphonate use. Maintenance of adequate calcium and vitamin D intake is crucial for all patients receiving bisphosphonate therapy.

Acknowledgments

We thank James M. Peterson for assistance with the figures.

Preparation of this article was supported by a Mayo Career Development Award to Dr Drake.

Dr Khosla has received research support from Procter & Gamble and has served on the advisory board for Novartis.

Glossary

  • ATP – adenosine triphosphate
  • BMD – bone mineral density
  • DXA – dual-energy x-ray absorptiometry
  • FDA – Food and Drug Administration
  • GIO – glucocorticoid-induced osteoporosis
  • HORIZON – Health Outcomes and Reduced Incidence with Zoledronic Acid Once Yearly
  • IV – intravenous
  • OI – osteogenesis imperfecta
  • ONJ – osteonecrosis of the jaw
  • PPi – inorganic pyrophosphate
  • PTH – parathyroid hormone
  • WHI – Women�s Health Initiative

Footnotes

Individual reprints of this article are not available.

According to the article above, although the utilization of bisphosphonates in clinical practice provides healthcare professionals with new treatment options for skeletal disorders,�further research studies are still required. Information referenced from the National Center for Biotechnology Information (NCBI).�The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

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Additional Topics: Acute Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain is the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.

 

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EXTRA IMPORTANT TOPIC: Chiropractic Hip Pain Treatment

What is Metastatic Bone Disease?

What is Metastatic Bone Disease?

Cancer which develops in specific organs of the human body, including the lungs, breast, or prostate, among others, can sometimes spread into the bone, causing what is known as�metastatic bone disease, or MBD. Approximately more than 1.2 million new cancer cases are diagnosed every year, where about 50 percent can spread,�or metastasize, to the bones.

Through medical advancements, patients diagnosed with several different types of cancers, especially lung, breast, and prostate cancer, can live longer. However, primary cancers in more patients go through bone metastases, where they disperse�to the bone. Meanwhile, other types of cancers do not disperse so easily to the�bone. The most common cancers which develop in the organs and spread to the bones include:

  • Breast
  • Lung
  • Thyroid
  • Kidney
  • Prostate

Metastatic bone disease,�or MBD, can damage�and weaken the affected bone, causing pain along the site of spread.�Moreover, patients with MBD are at higher risk of suffering fractures or broken bones. The painful symptoms associated with MBD can make it challenging for the patient to engage in regular physical activities. The main concern of patients with metastatic bone disease is the loss in quality of life.

The extent of the effects of metastatic bone disease on a patient can change and is associated with how cancer has spread, which bones are affected, and how severe the bone harm is. Furthermore, there is a range of treatment choices available to treat MBD. Treatment help patients deal with pain to maintain activity levels and preserve their independence.

Metastatic Bone Disease Explained

The bones are the most common site of spread for cancers which begin in the organs, subsequent to the lung and the liver. Because many patients experience no painful symptoms of metastases to the liver and the lungs, these are often not discovered until the disease is in an advanced stage. In contrast, bone metastases are generally painful when they develop. Cancer most commonly spreads to these sites in the human skeleton:

  • Skull
  • Spine
  • Ribs
  • Upper arm
  • Pelvis
  • Long bones of the leg

Bone Damage

A tumor can completely destroy the bone at the site of spread, a process referred to as osteolytic bone destruction. Damage or weakened bones are most common in cancers which have spread from the lung, thyroid, kidney, and colon. New bone,�called osteoblastic, may also form due to the spread of cancer, more often seen in cancers from the stomach, bladder, and prostate.

Breast cancer often behaves in a combined osteolytic and osteoblastic method. Since the cancer cells secrete factors that interact with all the cells in the human skeleton, causing bone destruction, new bone formation, or both, osteolytic and osteoblastic metastatic bone disease happens. Also, breast cancer may commonly cause MBD in the hip and/or pelvis.

As a result of bone damage and weakness, patients with�metastatic bone disease are prone to fractures. Broken bones caused by MBD are termed “pathological fractures”.�Sometimes, the bone may be so weak that a fracture is imminent, termed “impending pathologic fractures”. Bedrest for lengthy intervals due to broken bones may result in chemical imbalances in the bloodstream, such as raised calcium levels, known as hypercalcemia. Patients with cancer that has spread to the spine can develop nerve damage which can result in paralysis or loss of using their arms and/or legs.

MBD Symptoms

A cancer patient who experiences any pain, especially in the back, arms, and legs should notify their doctor immediately. Pain which manifests without engaging in physical activities is especially concerning. The most common symptoms of�metastatic bone disease include:

  • Pain: MBD’s most prevalent symptom is pain. Patients may experience pain along their hip and/or pelvis, upper and lower extremities, and spine because the tumor may have damaged or weakened the bone.
  • Fractures: Broken bones, or fractures, can range from mild to severe and are generally a clear indication of the presence of MBD.
  • Anemia: The most common sites of spread, skull, spine, ribs, upper and lower extremities, and hip and/or pelvis, correspond to regions of bone marrow which produce high levels of red blood cells, responsible for carrying oxygen to cells. Anemia, or decreased red blood cell production, is a frequent blood abnormality with MBD.

 

 

MBD Diagnosis

Before following through with treatment for metastatic bone disease, it’s essential for the healthcare professional to understand the patient’s symptoms as well as their overall health and wellness. The doctor will ask for the patient’s medical history. After the medical history, the healthcare professional will perform a physical examination on the patient. The doctor may also utilize imaging diagnostics to help with the patient’s diagnosis.

Imaging Diagnostics

  • X-rays:�After the initial diagnosis, they may order x-rays. Because pain may often originate from other regions of the body, the healthcare professional will also order x-rays beyond the regions where the patient is experiencing discomfort. X-rays may tell an oncologist a great deal of information regarding how much bone is affected.
  • Other imaging tests: The doctor may also order a bone scan. This test can determine if other bones are involved with metastatic bone disease. In select situations, a computerized tomography, or�CT, scan and magnetic resonance imaging, or MRI, may be ordered, especially in scenarios where the spine or hip and/or pelvis are involved.
Dr Jimenez White Coat

A variety of cancers can commonly cause metastatic bone disease, or MBD, throughout different regions of the human skeleton. Bone metastases can cause painful symptoms, ultimately affecting an individual’s quality of life. Research studies have demonstrated that metastatic bone disease in the hip and/or pelvis is a prevalent health issue associated with breast cancer. Treatment may vary on the progression of the problem.

Dr. Alex Jimenez D.C., C.C.S.T. Insight

Metastatic Bone Disease Treatment

Advances in surgical techniques, as well as radiation and medical treatment approaches, have significantly improved the quality of life of patients suffering from cancer that has spread to the bone from the site of origin. Treatment options for MBD are based upon how far the cancer has spread, which bones are affected, and how the bone was damaged or weakened.

In many cases of metastatic bone disease, cancer has progressed to multiple bony sites. As a result, treatment is concentrated on managing the symptoms of pain and bone weakness as it is not intended to be curative. The most common treatment option for MBD includes drugs and/or medications, and radiation to control pain and prevent additional spread of metastatic bone disease, and surgery to stabilize weak and broken bones.

Patients with metastatic bone disease require a team approach. A medical oncologist works closely with a radiation oncologist, and an orthopaedic surgeon. Diagnosis is essential in order to follow through with the best treatment approach. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

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Additional Topics: Acute Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain is the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.

 

 

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EXTRA IMPORTANT TOPIC: Chiropractic Hip Pain Treatment

Femoroacetabular Impingement

Femoroacetabular Impingement

Femoroacetabular impingement, or FAI, is a medical state where additional bone develops in a single or multiple of the bones which make up the hip joint, giving the bones an irregular form. As a result, the bones may rub against each other since they do not fit together properly. This friction can ultimately harm the joint, causing pain, discomfort and limiting movement.

Anatomy

The hip is commonly characterized as a ball-and-socket joint. The acetabulum, which is part of the large pelvis bone, forms the socket of the joint. The ball of the joint is the femoral head, that is the upper end of the thighbone or femur. A type of soft tissue, known as articular cartilage, covers the surface of the ball-and-socket hip joint.

Articular cartilage makes a smooth, low friction surface which aids the bones to slide easily across each other through movement. The acetabulum is also lined by strong fibrocartilage, known as the labrum. The labrum shapes a gasket across the socket, forming a tight seal to provide stability as well as to help properly support the hip joint.

With femoroacetabular�impingement, bone spurs or bone overgrowth, surround the femoral head, across the acetabulum. The extra bone causes the hip joints to come into close contact and prevents them from gliding smoothly and without friction during movements. With age, this can cause labrum tears and osteoarthritis, or the breakdown of articular cartilage.

Types of Femoroacetabular Impingement

According to doctors, there are three types of femoroacetabular impingement, or FAI: pincer, cam,�and combined impingement.

  • Pincer:�This variety of impingement develops when bone extends outwards from the standard rim of the acetabulum. As a result, the labrum is crushed beneath the rim of the acetabulum.
  • Cam: In cam,�impingement of the femoral head causes the joint to be unable to rotate smoothly. A bump forms on the border of the femoral head which grinds the cartilage inside the acetabulum.
  • Combined: Combined impingement suggests that both pincer and cam types of femoroacetabular�impingement are found.

Causes of FAI

Abnormal development of the hip bones and joints throughout childhood is the most common cause of femoroacetabular impingement. However, it is the deformity of a pincer bone spur�or a cam bone spur which leads to joint damage and hip pain. If the hip bones and joints do not form normally, there’s little which can be done to prevent femoroacetabular�impingement.

Many people may have FAI and never�experience symptoms from the condition. When symptoms develop, however, it generally indicates that there is damage to the cartilage or labrum and the health issue may progress. Moreover, athletes are more likely to experience symptoms of femoroacetabular impingement, although exercise does not cause FAI.

Symptoms of FAI

The most common symptoms of femoroacetabular impingement include: pain and discomfort; stiffness; and limping.�Pain associated with FAI frequently occurs in the region of the groin, although it may also occur toward the exterior of the hip. Twisting, turning, and squatting may cause a sharp, stabbing pain while the pain is generally described as a dull ache.

 

 

Diagnosis of FAI

For the first consultation, the healthcare professional will discuss the patient’s hip symptoms and talk about their general health and wellness. They will also examine the patient’s hip. As part of the physical evaluation, the doctor will conduct an FAI impingement test by bringing up the patient’s knee then rotating it towards their opposite shoulder. If this recreates hip pain, the test is positive for femoroacetabular impingement.

Imaging Diagnostics

The healthcare professional may also order imaging diagnostics to help determine whether the patient has femoroacetabular impingement, or FAI. The following imaging diagnostics below can be used.

  • X-rays: These will show whether the hip has shaped bones of FAI, and provide images of the bone. X-rays may also reveal signs of arthritis.
  • Computed tomography (CT) scans: More comprehensive than a plain x-ray, CT scans help the healthcare professional determine the specific contour of the patient’s hips.
  • Magnetic resonance imaging (MRI) scans: These tests create pictures of soft tissue. They will help the doctor find harm to the labrum and articular cartilage. Injecting dye into the joint may make the damage or injury show up more clearly.
  • Local anesthetic: The doctor can also inject a numbing medication into the hip joint as a test. It affirms that FAI is the problem if temporary pain relief is provided by the local anesthetic.
Dr Jimenez White Coat

Femoroacetabular impingement, or FAI, commonly affects the hip joint of many young and middle-aged adults. FAI occurs when the ball-and-socket joint of the hip causes abnormal friction and restricts range of movement. Furthermore, damage or injury to the articular cartilage or the labrum can affect the femoral head or the acetabular socket. Treatment options for FAI can range from alternative treatment options to surgery.

Dr. Alex Jimenez D.C., C.C.S.T. Insight

Treatment for Femoroacetabular Impingement

Non-Surgical Treatment

  • Lifestyle modifications:�The healthcare professional may recommend changes in physical activities that cause symptoms, simply altering the patient’s regular everyday routine.
  • Drugs and/or medications: The use of drugs and/or medications, such as ibuprofen, can be offered to help decrease painful symptoms and inflammation. The relief may only be temporary.
  • Alternative treatment options:�Treatment approaches like chiropractic care and physical therapy can help provide pain relief to patients with femoroacetabular impingement. Moreover, specific stretches and exercises can strengthen the muscles which support the joint and can boost range of movement. This can help relieve some stress and pressure on articular cartilage or the labrum.

Surgical Treatment

If imaging diagnostics and physical evaluations reveal additional hip joint damage and/or injury as well as the presence of other conditions and non-surgical treatment does not relieve the patient’s pain, the healthcare professional may recommend surgical interventions or surgery.

Arthroscopy

Femoroacetabular impingement can be treated with arthroscopic surgery. Arthroscopic surgical interventions are performed with thin instruments using little incisions. The surgeon then utilizes a small camera to look�inside the hip. The doctor can fix or clean out any damage to the labrum and articular cartilage by shaving the bulge on the femoral head and also trimming the bony rim of the acetabulum.

As the results of operation enhance, physicians will recommend surgery that is earlier for FAI. Surgical techniques continue to progress and at the future, computers may be utilized to guide the physician in reshaping and correcting the hip. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

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Additional Topics: Chiropractic for Athletes with Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain is the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.

 

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EXTRA IMPORTANT TOPIC: Piriformis Syndrome Chiropractic Treatment

Bisphosphonate-Related Proximal Femoral Fractures

Bisphosphonate-Related Proximal Femoral Fractures

With the increase of osteoporosis in older adults, the diagnosis and treatment�of abnormal hip fractures, such as�bisphosphonate-related proximal femoral fractures,�has become more important. According to Dr. Edward J. Fox, MD, obesity is often managed through the long-term�use of bisphosphonate treatment, which can inhibit�osteoclast-mediated bone regeneration. Over the prolonged utilization of bisphosphonate, patients� may develop atypical proximal femoral fractures.

Understanding Atypical Femur Fractures

Atypical femur fractures are characterized as stress fractures which commonly occur in the proximal one-third of the diaphyseal bone, although they might also occur more distally, developing in the lateral cortex and slowly progressing medially. “With irregular fractures, a small ‘beak’ of bone can form on the lateral surface of the femur and that is where the fracture generally begins,” explains Dr. Fox. This contrasts with stress fractures which occur laterally in the medial portion of the bone.

As a result, when a patient with osteoporosis reports feeling hip and knee pain without previous damage or injury, healthcare professionals will ask about bisphosphonate treatment. It is essential for the�doctor to request x-rays of the hip and femur shaft for proper diagnosis.�It is also important to request x-rays of the opposite femur, as atypical bisphosphonate-related proximal femoral fractures frequently occur bilaterally. Dr. Edward J. Fox urges patients to discontinue bisphosphonate use in the case of hip fractures,�followed by the subsequent use of crutches or a walker. Patients will eventually be able to resume regular physical activities.

 

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Approximately more than 250,000 hip fractures occur in the United States, causing significant patient disability. The variety of hip fractures in older adults, including bisphosphonate-related proximal femoral fractures, often need several treatment approaches which depend on different considerations, such as the mechanism of injury, location and degree of the fracture, as well as the patient’s age and overall health and wellness.

Dr. Alex Jimenez D.C., C.C.S.T.

 

 

The precise mechanism of injury by which bisphosphonates cause atypical femur fractures is unknown. Research studies have demonstrated that the suppression of osteoclast activity prevents the clearance of bone fragments which build up on the bone surface during regular daily tasks; decreasing the strength of the bones which lead to fracture. “We all know that the threat of those fractures increases with the extended duration of bisphosphonate exposure, particularly after five decades. Bisphosphonates are stored with a half-life of at least eight decades in bone matrix. To reduce over-exposure and risk of atypical fracture, passing medication discontinuance has been speculated to be beneficial,” explained Dr. Fox

Dr. Edward J. Fox, MD, stated that until research studies find the exact mechanism of injury and treatment for bisphosphonate-related proximal femoral fractures, healthcare professionals should continue to determine the best treatment option for each patient, carefully weighing the benefits and risks of individual patients. The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

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Additional Topics: Acute Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain is the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.

 

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EXTRA IMPORTANT TOPIC: Chiropractic Hip Pain Treatment

Impacted Femoral Neck Fractures

Impacted Femoral Neck Fractures

Hip fractures are characterized as any type of break in the upper region of the femur or thigh bone. The variety of broken bones generally depends on the circumstances and the force applied to the bone, where some can be more common than others. Impacted femoral neck fractures are common hip fractures which occur in many older adults in the United States.

Anatomy of Impacted Femoral Neck Fractures

The hip is a ball-and-socket joint which provides the femur the ability to bend and rotate at the pelvis. While any form of broken bones in the thigh bone or femur is considered a hip fracture, damage or injury to the socket, or acetabulum, itself is not considered a hip fracture. Below we will discuss hip fractures, particularly impacted femoral neck fractures, among others.

Causes, Symptoms and Diagnosis

Hip fractures frequently�occur due to a slip-and-fall accident or due�to a direct blow to the hip. Various health issues, including osteoporosis and stress injuries, as well as cancer, can sometimes weaken the bones and make the pelvis more vulnerable to fractures.�The neck of the femur is located under the ball of the hip joint. Impacted femoral neck fractures occur when a force presses against both ends of the femur at the femoral neck, pushing the broken ends of the bone together.

Patients with hip fractures experience symptoms of pain on the upper thigh or in the groin. They may also experience considerable discomfort with any attempt to flex or rotate the hip. In comparison to impacted femoral neck fractures, if the bone is completely broken, the leg may appear to be shorter than the non-injured leg. Also, the patient will hold the injured leg in a still position with the foot and knee turned outward in external rotation.

Diagnosis�for hip fractures commonly involves the use of x-rays of the hip, pelvis and/or femur. In several instances, if the patient experiences a slip-and-fall accident or a direct blow to the hip resulting in impacted femoral neck fractures, they may not be seen on a regular x-ray. Magnetic resonance imaging, or MRI, may be recommended to view some cases of hip fractures. The MRI scan will typically demonstrate any hidden hip fractures. Computed tomography, or CT, scans may also be utilized instead.

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Impacted femoral neck fractures are hip injuries which occur just below the femoral head, or the ball-and-socket hip joint, where the broken ends of the bone are jammed together by the force of the injury. This area of the thigh bone, or femur, is known as the femoral neck. Treatment for impacted femoral neck fractures may include rest and physical rehabilitation. Diagnosis for impacted femoral neck fractures is important for treatment.

Dr. Alex Jimenez D.C., C.C.S.T.

 

 

Treatment of Impacted Femoral Neck Fractures

Once a healthcare professional has diagnosed the patient’s hip fracture, their overall health and wellness will also be evaluated.�Treatment for femoral neck stress fractures depends on the patient’s age and on the extent of the broken bone. Treatment for femoral neck stress fractures�include bed rest for several days followed by a physical rehabilitation program.

Many femoral neck stress fractures are treated with surgery. It’s essential for the patient to talk to their doctor to discuss the best treatment option.�The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

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Additional Topics: Chiropractic for Athletes with Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain is the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.

 

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EXTRA IMPORTANT TOPIC: Chiropractic Hip Pain Treatment

Femoral Neck Stress Fractures

Femoral Neck Stress Fractures

The hip is a ball-and-socket joint composed of the head of the thigh bone, or femur,�which acts as the ball and fits into the round socket of the hip bone, or acetabulum. The neck of the femur is located under the ball of the hip joint. Stress fractures to the femoral neck can entirely or partially detach the femoral head from the rest of the femur.

Femoral neck stress fractures can be either displaced, where the bone is transferred out of its normal position, or non-displaced, where the bone remains stable. These fractures may interrupt blood flow to the portion of the broken bone. In recovery, the blood supply prevents severely displaced femoral neck stress fractures from healing correctly.

Causes and Symptoms of Femoral Neck Stress Fractures

Femoral neck stress fractures can result due to: a small slip-and-fall accident or twisting of the hip in older adults, osteoporosis, a high-impact�injury, such as from an automobile accident, and�sudden strenuous physical activity or changes in physical activity in younger individuals unaccustomed to the events, including from sports injuries.�

The symptoms of femoral neck stress fractures generally include: pain and discomfort, radiating pain which extends to the knee, inability to bear weight on the affected lower extremity, shortening or sideways rotation of the leg, increased pain in the hip during the rotation of the leg, and inflammation on the side of the hip with the femoral neck stress fractures.

 

 

Diagnosis and Treatment of Femoral Neck Stress Fractures

A healthcare professional will diagnose femoral neck stress fractures based on the causes and symptoms of the health issue, followed by clinical evaluation. Many doctors order x-rays to diagnose femoral neck stress fractures. The doctor may also order�magnetic resonance imaging, or MRI, and computer tomography, or CT, scanning for a better diagnosis.

Treatment for femoral neck stress fractures depends on the patient’s age as well as on the extent of the broken bone. Treatment for femoral neck stress fractures may include�bed rest for several days followed by a physical rehabilitation program. A healthcare professional may prescribe drugs and/or medications to relieve pain, prevent blood clots and treat infection.

Many femoral neck stress fractures are treated through surgical interventions. Surgery for femoral neck stress fractures involves hip pinning if the bone is minimally displaced and the patient has�enough bone density. The surgeon performs this by making a small incision and then inserting several screws to stabilize the bones which are broken.

Hip hemiarthroplasty or partial hip replacement is utilized for displaced fractures where the surgeon will replace the�femoral head with a metal implant. The socket is not replaced in a partial hip replacement procedure. For total hip replacement, the surgeon will replace the socket of the hip joint, as well as the femoral head, with artificial metallic implants.

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Femoral neck stress fractures are hip injuries which occur just below the femoral head, or the ball-and-socket hip joint. This area of the thigh bone, or femur, is known as the femoral neck. Femoral neck stress fractures happen when the ball is disconnected from the rest of the femur, or thigh bone. Treatment for this health issue includes rest and physical rehabilitation.

Dr. Alex Jimenez D.C., C.C.S.T.

Conclusion

Femoral neck stress fractures occur�in the hip area below the ball-and-socket joint of the hip. A healthcare professional will suggest treatment based on the severity of the femoral neck stress fractures and the patient’s age.�The scope of our information is limited to chiropractic as well as to spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at�915-850-0900�.

Curated by Dr. Alex Jimenez

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Additional Topics: Chiropractic for Athletes with Back Pain

Back pain�is one of the most prevalent causes of disability and missed days at work worldwide. Back pain is the second most common reason for doctor office visits, outnumbered only by upper-respiratory infections. Approximately 80 percent of the population will experience back pain at least once throughout their life. The spine is a complex structure made up of bones, joints, ligaments, and muscles, among other soft tissues. Because of this, injuries and/or aggravated conditions, such as�herniated discs, can eventually lead to symptoms of back pain. Sports injuries or automobile accident injuries are often the most frequent cause of back pain, however, sometimes the simplest of movements can have painful results. Fortunately, alternative treatment options, such as chiropractic care, can help ease back pain through the use of spinal adjustments and manual manipulations, ultimately improving pain relief.

 

blog picture of cartoon paper boy

 

EXTRA IMPORTANT TOPIC: Chiropractic Hip Pain Treatment