Keywords

2.1 Introduction

The main consequence of osteoporosis is that it is a condition in which bone mass is depleted and bone structure is destroyed to the degree that bone becomes fragile and prone to fractures. For affected patients, these ‘fragility fractures’ are associated with substantial pain and suffering, disability and even death, along with substantial costs to society [1]. The problems created by fragility fractures and osteoporosis are multifactorial in origin and are, therefore, an interdisciplinary problem. A first fragility fracture is often the first sign of osteoporosis, and ‘secondary’ prevention of fragility fractures is focused on the prevention of further fractures once an initial fracture has occurred.

The global prevalence of osteoporosis is estimated at 20% with variation between countries and continents [2]. The number of people suffering from osteoporosis (with high risk of fractures) is increasing significantly over time, probably because of global ageing and longer life expectancy, leading to a higher prevalence of osteoporosis and fractures in the general population.

Nurses, alongside other practitioners, play a key role in the education and guidance of patients with osteoporosis and prevention of fragility fractures. This chapter provides an overview of how osteoporosis and fragility fractures are linked, with a focus on fracture prevention.

2.2 Learning Outcomes

At the end of the chapter, and following further study, the nurse will be able to

  • Explain the fundamentals of bone biology and its relevance to osteoporosis and fragility fractures.

  • Describe the most common fragility fractures, their epidemiology and impact on individuals.

  • Undertake fracture risk assessment using different calculation tools (e.g. FRAX©, Garvan) and recognise and modify the fixed and modifiable risk factors.

  • Educate communities and individuals about osteoporosis diagnosis, treatment and advise on lifestyle changes.

  • Outline the overall goal and benefits of osteoporosis treatment and support individuals during treatment.

2.3 Bone Biology

The human skeleton gives structure to the body, protects organs, makes motion and mobility possible by attachment to muscles via tendons and ligaments, stores and releases minerals and, in the bone marrow, manufactures blood cells. About 80% of the skeleton is cortical (or compact) bone, which forms the outer structure of the shafts of long bones. Trabecular bone (20%) is mainly present in the ends of long bones and in the centre of the vertebrae and ribs. Bone undergoes a lifelong process of replacement, with mature bone being replaced with new. This regulated process of ‘bone turnover’ maintains a balance between bone resorption and formation to maintain skeletal integrity [3]. This occurs throughout a person’s life, resulting in a replacement of 5–10% of the total skeleton each year and a total renewal of the skeleton every decade [4].

Remodelling involves three types of cells: osteoblasts (bone builders), osteoclasts (bone eaters) and osteocytes (‘directors’ of bone remodelling and repair). There is a continuously ongoing interaction between hormones, minerals and bone cells that is influenced by:

  1. 1.

    Changes in calcium levels in the blood

  2. 2.

    Pressure/strain on bones generated by gravity and the action of muscles

  3. 3.

    Hormones (oestrogen, testosterone and growth hormone)

In youth, bone formation exceeds resorption, so bone mass and strength increase. Peak bone mass is achieved at an age of 20–25 years [5]. At 30–40 years, bone mass gradually decreases as bone resorption exceeds bone formation. By the age of 80, it is estimated that total bone mass is +/− 50% of its peak [6]. When the balance tips towards excessive resorption, bones weaken (osteopenia) and, over time, can become brittle and at risk of fracture (osteoporosis) [7]. See Fig. 2.1.

Fig. 2.1
A photo of 3 cuboidal bone structures. A. Densely packed irregular pores in the bones. B. Lightly packed pores. C. Thick threads of bones intertwined with each other.

The progression from healthy bone to severe osteoporosis: (a) healthy bone, (b) osteoporosis, (c) severe osteoporosis

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2.4 Osteoporosis

Osteoporosis is a common, chronic, systemic skeletal disease that is ‘characterised by low bone mass and microarchitecture deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture’ [8]. See Fig. 2.1. It is a devastating condition that can lead to pain, severe disability and premature death from fracture. As bones become more porous and fragile, the greater the increase in the risk of fracture. Patients are often unaware that they are at risk of or have osteoporosis as bone loss occurs silently and progressively without signs or symptoms until fractures occur.

2.4.1 Epidemiology

Osteoporosis is a global problem, but the size of the problem is unclear because of the variability in assessment and awareness, which probably leads to erroneously low reporting. However, epidemiological studies report extremely high estimated figures:

  • Worldwide, it is estimated that 200 million women suffer from osteoporosis [9] and 1 in 3 women and 1 in 5 men will experience a fragility fracture resulting in a hospital visit every 3 s.

  • In 2010, in the EU alone, 22 million women and 5.5 million men were estimated to have osteoporosis, resulting in 3.5 million new fragility fractures comprising:

    • 610,000 hip fractures

    • 520,000 vertebral fractures

    • 560,000 forearm fractures

    • 1.8 million other fractures [10]

  • The economic burden of fractures was estimated at €37 billion and is still rising [10].

  • After a fracture, the overall risk of a subsequent fracture is doubled, but this fluctuates over time and the risk is highest immediately after an initial fracture [11].

  • Regarding the clinical consequences of fracture, for example after hip fracture:

    • 40% cannot walk independently.

    • 80% cannot perform basic activities such as shopping independently.

    • 10–20% require permanent residential care [12].

  • By 2050, the worldwide incidence of hip fracture is believed to increase threefold in men and double in women [13].

  • The number of people living with osteoporosis in all regions of the world will increase dramatically in the coming decades due to ageing populations and lifestyle changes that are bone-unhealthy.

2.4.2 Fragility Fracture

‘Fragility fractures occur as a result of “low-energy” trauma, often from a fall from standing height or less, that would not normally result in a fracture’ [14] and are a major public health problem; one occurs globally every 3 s, with high human and socio-economic impact, morbidity, mortality and costs [15].

For individuals, fractures frequently result in loss of autonomy, deterioration in quality of life and need for care [8]. A fragility fracture may result from minimal trauma (e.g. a fall from a standing height) or no identifiable trauma at all [12]. The fracture is both a sign and a symptom of osteoporosis and a predictor for subsequent fractures [11].

Typically, fractures in patients with osteoporosis occur at the following locations [17]

  • Vertebral (spine)

  • Proximal femur (hip)

  • Distal forearm (wrist)

  • Proximal humerus

Wrist or distal forearm fractures are the third most common type of osteoporotic fractures [16], accounting for up to 18% of all fractures among older people [17], and their impact on quality of life due to complications and impaired function is often underestimated [18]. Distal forearm fractures are usually ‘the first’ fragility fracture, frequently followed by a subsequent hip or vertebral fracture [19].

Hip fractures are the most serious fractures in terms of cost and morbidity. Although a woman’s risk of dying from a hip fracture is high (and exceeds the lifetime risk of death from breast cancer, uterine cancer and ovarian cancer combined), the mortality risk after a hip fracture is much higher for men. Hip fracture nearly always requires hospitalisation and is fatal in almost a quarter of all cases. For those who survive after a hip fracture, most do not regain their pre-injury level of function and 30% experience loss of independence. Dependency is greatly feared by patients and is costly to their family and to society [20]. If a first fragility fracture is recognised and osteoporosis treated, the risk of a future fracture can be reduced, preventing the continued downward spiral in health and quality of life, and even death, that often follows hip fracture [21].

Vertebral fractures are the most common manifestation of osteoporosis and are usually diagnosed when a patient presents with back pain, with a spinal X-ray showing vertebral body fracture. Vertebral fractures are 65–75% asymptomatic, or mildly symptomatic, and only 30–40% come to medical attention at the time that they occur [22]. Vertebral fractures in older adults are associated with increased mortality, often due to their association with frailty (see Chap. 3) [23]. A vertebral fracture increases the risk of sustaining more vertebral fractures, a phenomenon often referred to as ‘vertebral fracture cascade’. Recognised vertebral fractures are usually treated non-surgically with a brief period of rest (bed), pain medication, bracing and physiotherapy. Approximately 40% of patients develop chronic disabling pain and/or spinal deformity (kyphosis) resulting in reduced pulmonary function that is associated with increased risk of mortality. Vertebral fractures increase the risk of sustaining future fractures fivefold, so it is important to identify them and immediately start preventive treatment. If a vertebral fracture occurs when patients are already being treated for osteoporosis, therapy will require evaluation and adjustment.

It is important to identify patients who are at increased risk of fracture. It has been estimated that only 20–30% of people sustaining a fragility fracture gain access to preventive care, despite international evidence that shows that a systematic approach to secondary prevention provided by ‘fracture liaison services’ results in fewer fractures and significant cost savings (see Chap. 5). Nurses and other practitioners can play a key role in identifying risk factors and providing education about the importance of a fracture risk assessment and fracture prevention. This can be done regardless of whether the practitioners work in hospital-based, homecare or residential care settings. Regarding fracture prevention, it is important to assess the patient’s knowledge of osteoporosis and provide education regarding lifestyle factors such as calcium-rich diet and exercise. Practitioners should also assess any potential barriers such as limited access to healthy food, impaired mobility, impaired health literacy or language barriers.

Investing in fracture risk assessment and education about fracture risk reduction is an important area of potential interventions that are within the scope of daily clinical care. Nurses and other practitioners can play an important role in the management of patients with osteoporosis through supporting self-management in a way that is agreeable to patients and their family. Measures can be planned to impact modifiable risk factors and meet the individual’s need for information and education. Secondary fracture prevention is discussed in significant detail in Chap. 5.

2.4.3 Risk Factors

Many risk factors for osteoporosis and fractures have been identified. They can be divided into two categories: fixed and modifiable. Fixed risk factors (listed in Box 2.1) cannot be modified but help to identify patients with high fracture risk [24].

Box 2.1 Fixed Risk Factors for Osteoporosis [24]

Age: Above 50 years of age contributes to risk of fracture independently of BMD (bone mineral density), with doubling of risk for every decade thereafter.

Female gender: Women are more at risk of developing osteoporosis due to menopausal decrease in oestrogen. Women have a lower peak bone mass than men.

Parents with a hip fracture: Having a parent with a hip fracture at any time in their lives is associated with an increased risk of fracture (independent of BMD).

Previous fracture: At least one earlier fracture that occurred in adult life—or a fracture arising from trauma which, in a healthy individual, would not have resulted in a fracture—doubles the risk of a second fracture in both men and women.

Ethnicity: Caucasian and Asian people have a higher incidence of osteoporosis and fractures of the hip and spine.

Menopause: Osteoclasts are more active, and bone loss increases due to decrease in oestrogen levels following menopause or oophorectomy.

Long-term glucocorticoid therapy: (>5 mg/day of prednisone or equivalent for >3 months) increases bone loss and impairs bone formation—calcium absorption is affected and muscle weakness can occur, increasing the risk of falling.

Rheumatoid arthritis (RA): Inflammatory cytokines and impaired mobility increase bone loss; people with RA have a twofold risk to have osteoporosis.

Primary/secondary hypogonadism in men: Due to hormone disorders, normal ageing or androgen deprivation therapy in prostate cancer—rapidly increases bone loss.

Secondary risk factors: Disorders and medications that make the bone more fragile and/or affect balance and risk of falling.

Most modifiable risk factors (listed in Box 2.2) directly impact bone biology and result in a decrease in bone mineral density but can also increase the risk of fracture independently of their effect on bone itself. Practitioners can educate and guide individuals towards healthier lifestyles to reduce these risk factors as much as possible (see Chap. 5).

Box 2.2 Modifiable Risk Factors for Osteoporosis [24]

Alcohol: Excessive alcohol consumption (>3 U daily) increases the risk of a fracture by 40% due to direct adverse effects on osteoblasts and parathyroid hormone levels (regulates calcium metabolism), associated with poor nutritional status (calcium, protein and vitamin D deficiency) [25].

Smoking: Current and/or past smoking; the exact mechanism is unknown, but increased fracture risk is reported when there is a history of cigarette smoking [26].

Low body mass index (BMI): Regardless of age, sex and weight loss, BMI <20 kg/m2 is associated with a twofold increased risk of fracture.

Poor nutrition with low dietary calcium intake: Inadequate intake of calcium, vitamin D or both influences calcium-regulating hormones; deficiency of either calcium or vitamin D will result in impaired calcium absorption and lower concentration of circulating calcium; parathyroid hormone (PTH) secretion is stimulated, increasing PTH levels, leading to an increase in bone remodelling, significant loss of bone and increased risk of fracture (see Chap. 11).

Vitamin D deficiency: Vitamin D plays an essential role in calcium absorption; it is made in the skin when exposed to the sun’s ultraviolet rays (10−15 min a day is usually sufficient); food sources (see Chap. 11) or supplemental sources of vitamin D are beneficial [27].

Eating disorders: Due to poor nutrition and vitamin D deficiency, there is a risk of obtaining a lower peak bone mass in early adulthood.

Oestrogen deficiency: Accelerates bone loss and reduces the build-up of bone mass; related to both hormone imbalance (e.g. early menopause) and nutritional factors.

Frequent falls: For factors that increase the risk of falling (see Chap. 4).

Sedentary lifestyle: Physical activity and fitness reduce the risk of osteoporosis and fracture as well as other fall-related injuries [28].

Low bone mineral density, one of the most important indicators of fracture risk, is both a fixed and modifiable risk factor. Many cross-sectional and prospective population studies indicate that the risk for fracture increases by a factor of 1.5–3.0 for each standard deviation decrease in bone mineral density [29]. Bone mineral density is determined by a wide range of factors including family history, age and lifestyle. Prevention of osteoporosis starts in youth by gaining sufficient peak bone mass; it is estimated that a 10% increase in the peak bone mass of children reduces the risk of an osteoporotic fracture during adulthood by 50% [30]. Lifestyle choices influence 20–40% of the reached peak bone mass [31], so lifestyle factors known to influence peak bone mass and strength are an important strategy to reduce the risk of developing osteoporosis or fractures later in life. Children should be encouraged to exercise and play outside and should be given vitamin D supplements (according to national guidelines) alongside a healthy diet with sufficient calcium intake. When an individual is diagnosed with osteoporosis, prevention is no longer about gaining a higher bone mass, but preventing fractures. Treatment of osteoporosis consists of prescription of specific anti-osteoporosis medication and calcium and vitamin D supplements in combination with healthy lifestyles.

2.4.4 Diagnosis

Diagnosis and treatment of osteoporosis include a five-step approach: (1) case finding, (2) risk evaluation, (3) differential diagnosis of secondary osteoporosis, (4) therapy/treatment and (5) follow-up [32].

2.4.4.1 Case Finding

Case finding involves opportunistically identifying patients with osteoporosis when they present with a first fracture, using the fracture (a risk factor itself) as the starting point. This is the first step towards identifying those patients most urgently in need of fracture prevention through one of the two approaches:

  • Primary prevention: Preventing the first fracture by identifying patient risk factors and starting treatment; often in primary healthcare settings where there may be a lack of structured or organised programmes. The presence of risk factors for osteoporosis, such as a family history of osteoporosis, fragility fracture, ethnicity, age, smoking history and alcohol consumption can be assessed by nurses and other practitioners, as well as a physical assessment identifying people with small body frame and/or low weight or BMI, loss of height and kyphosis.

  • Secondary prevention: Preventing a second fracture after the first; assessment and treatment are performed in hospitals using structured programmes such as fracture liaison services (FLSs) (Chap. 5) and often initiated in the emergency department (ED).

2.4.4.2 Risk Evaluation and Diagnosis of Osteoporosis

The diagnosis of osteoporosis is made by measuring bone mineral density (BMD) using dual-energy X-ray absorptiometry (DXA). Low BMD is the strongest risk factor for fracture. Clinical diagnosis of osteoporosis is based on BMD measurements and presence of fractures [33]; BMD is described, for diagnosis and risk estimates, in terms of T-scores, i.e. the number of standard deviations that separate the BMD of the individual from the average BMD of healthy young adults of the same gender and race (peak bone mass). The WHO thresholds for each bone category are shown in Table 2.1.

Table 2.1 WHO criteria for clinical diagnosis of osteoporosis [33]
Full size table

The DXA scan gives an estimation of bone strength by measuring the BMD in g/cm2 in an area of the lumbar spine (L1–4), proximal femur and hip with little or no radiation exposure (20 μSv). A pictorial example is provided in Fig. 2.2. DXA measurements can be negatively influenced by failing to position the patient properly, recent ingestion of barium for abdominal investigation, presence of vertebral fractures in the L1–4 region, hip prostheses, degenerative skeletal problems and severe arterial calcifications.

Fig. 2.2
A diagram of normal bone with tightly packed tiny pores, osteopenia with larger pores, and osteoporosis with enlarged pores, reflecting different T scores from negative 1 S D or more to negative 2.5 or less.

Comparative view of normal bone, osteopenia and osteoporosis indicating links to T-score results. (Reproduced under the terms of the ‘Creative Commons Attribution’ for Open Access content CC BY 4.0)

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Most DXA scanners can also undertake an additional investigation of the spine at the same time, known as vertebral fracture assessment (VFA). The results are methodically assessed according to the Genant Classification [34]. The presence of a vertebral fracture is always a sign of impaired bone strength, a predictor of a next fracture and an indication for treatment. Vertebral fractures can also be identified by X-ray when VFA is inconclusive or not available.

2.4.4.3 Assessment Calculation Tools

Until recently, the strategy for preventing fractures was based on the performance of DXA and verification of the WHO densitometry criteria: those with normal or osteopenic values were given preventive measures, and those with osteoporosis were additionally eligible for pharmacological treatment [35]. The limitations of this approach were well recognised. In fact, most fractures occur among people with BMD values in the non-osteoporotic range, who would be excluded from treatment under this paradigm. Additionally, several risk factors for fracture were identified which were independent of BMD [36]. This led, though numerous and careful meta-analyses of data on risk factors, to the development of risk assessment tools, which can be used to estimate the future absolute fracture risk in the individual patient, based on clinical variables, with or without DXA. The most widely used of these is the FRAX®, but others have been developed, including the QFracture® and the Garvan risk calculator [37].

The FRAX®, launched in 2008, was developed by the WHO Collaborating Centre for Metabolic Bone Diseases at Sheffield, UK. It is an algorithm that estimates the probability of a fragility fracture occurring in a given individual over the subsequent 10 years, based on clinical risk factors (age, body mass index and dichotomised risk factors comprising prior fragility fracture, parental history of hip fracture, current tobacco smoking, long-term oral glucocorticoids, rheumatoid arthritis, causes of secondary osteoporosis and alcohol consumption) [38]. It may be performed with or without information on BMD and considers mortality in the same population as a competing risk. All these risk factors have been shown to be significant predictors of fracture in the presence or absence of BMD values, although their specific impact varies according to whether BMD is or is not considered. This algorithm is available online, in multiple languages with country-specific calibration to the national epidemiology of fracture and mortality of many countries worldwide.

2.4.4.4 Differential Diagnosis of Secondary Osteoporosis

Approximately 30% of women and 50% of men with osteoporosis have secondary osteoporosis that may be known or hidden and is caused by specific clinical conditions (Box 2.3). Treating the cause can decrease fracture risk and avoid unnecessary treatment [39], so every patient with a fragility fracture and a low BMD should have a baseline blood test for bone and mineral metabolism (calcium, phosphate, alkaline phosphatase, 25-hydroxyvitamin D, parathyroid hormone, kidney function, full blood count and thyroid-stimulating hormone).

When individuals are already living with a specific clinical condition (Box 2.3) that is associated with osteoporosis, it is important to promote evaluation by diagnostic tools and provide education on osteoporosis, fracture risk and lifestyle factors known to influence the risk of developing osteoporosis and fractures.

Box 2.3 Examples of Disorders Associated with Secondary Osteoporosis

  • Diabetes mellitus

  • Cushing’s syndrome

  • Hyperparathyroidism

  • Hyperthyroidism

  • Premature menopause

  • Hypogonadism

  • Celiac disease

  • Inflammatory bowel disease

  • Liver cirrhosis

  • Rheumatoid arthritis

  • Ankylosing spondylitis

  • Systemic lupus erythematosus

  • Anorexia nervosa

2.4.5 Treatment

Many patients are unaware that they have osteoporosis until after their first fracture, but even after a fracture, it often goes untreated. What is known as the international ‘treatment gap’ is that fewer than 20% of those who sustain a fragility fracture receive therapies to reduce the risk of fracture within the year following the fracture [40]. Preventive treatment has no effect on symptoms so may not be attractive to patients who may prioritise symptom control and a low treatment burden. Before treatment is even discussed, healthcare professionals must be aware of what the individual’s baseline understanding about osteoporosis is and what their preferences are regarding fracture-reducing treatment. Treatment of osteoporosis is always a combination of medication, lifestyle choices, adequate intake of calcium and vitamin D and prevention of falls.

The goal of treatment, including osteoporosis medication, is to prevent fractures (not to increase the DXA numbers). Fracture risk can be reduced with optimal treatment of osteoporosis that consists of:

  • Specific anti-osteoporosis medication (agreed on through shared decision-making)

  • Adequate intake of calcium and vitamin D (dietary or supplements)

  • Attention to lifestyle factors (must go hand in hand with any drug treatment prescribed)

  • Fall prevention (when relevant)

  • Follow-up (a plan that is known by the patient)

2.4.5.1 Medication to Reduce Fracture Risk

There are various medications to treat osteoporosis, all having different entry points, but they all have the same goal: preventing fractures. It should be noted that not all types of medication are available in all countries or regions worldwide. The most common approved treatments will be considered here including:

  • Bisphosphonates (alendronate, ibandronate, risedronate and zoledronic acid) (oral or intravenous)

  • ‘Selective oestrogen receptor modulators’ (SERMs) (raloxifene, bazedoxifene; oestrogen ‘agonist/antagonist’ drugs that act like oestrogen in bone, but in the uterus and breast tissue act like an oestrogen blocker)

  • Monoclonal antibody (denosumab): reduces bone turnover by inhibiting the maturation of osteoclasts (subcutaneously every 6 months)

Bone-building therapies are

  • Teriparatide: a synthetic form of parathyroid hormone (PTH) that stimulates (new) bone formation, resulting in increased BMD:

    • Daily subcutaneous injection for 24 months

  • Abaloparatide: an analogue of human parathyroid hormone-related protein (PTHrP):

    • Daily subcutaneous injection for 24 months

  • Romosozumab: a monoclonal antibody that promotes bone formation and inhibits bone resorption:

    • Two subcutaneous injections every month for 12 months

While the development of new treatments is ongoing, the most commonly prescribed are bisphosphonates which attach to bone tissue and reduce bone turnover by suppressing the activity of osteoclasts, often referred to as ‘anti-resorption’ therapy. The drug must be taken regularly for a minimum of 3–5 years initially and is combined with calcium and vitamin D supplements. Oral bisphosphonates are poorly absorbed (only approximately 1% of each dose), even with total compliance and proper administration. When administered orally, bisphosphonates must be taken according to the following instructions:

  • In the morning on an empty stomach.

  • At least 30 min before any food or drink.

  • Swallowed whole with a large glass of tap water.

  • The patient must remain upright for at least 30 min.

  • Any calcium-containing supplements must be delayed for 3–4 h.

2.4.5.2 Follow-Up

Proper follow-up improves adherence and compliance with treatment and facilitates monitoring of the treatment goal: fracture prevention. At the start of the treatment, patients must be aware of the duration, the goal and benefits, for how long the medication must be taken and from whom to seek support when problems, such as side effects, occur. The occurrence of a fracture in patients on treatment is always a reason to re-evaluate treatment strategies, especially when this includes a vertebral fracture. Many patients fail to persist with their treatment, and many others experience a suboptimal response due to unintentional poor compliance or impaired absorption. Approximately 50% of all patients who start treatment stop within the first year [41].

It is important to check regularly that patients are following the instructions and are continuing to take their treatment properly. Despite the wishes of most patients to measure the effect of the treatment short-term, it is not recommended to make periodic measurements of BMD by DXA because BMD changes because of osteoporosis treatment occur slowly and the magnitude of measurement error with DXA is similar to the short-term change in response to treatment. An alternative approach is to measure biochemical markers of bone turnover in blood samples. These show large and rapid changes in response to osteoporosis treatment, allowing detection of a significant treatment response within a few months.

Another factor in poor compliance is fear of side effects. In oral treatments, gastrointestinal complaints are a common reason for patients to stop the treatment without talking to their health practitioner. It is important that patients report side effects so that further treatment options can be discussed. A rare, but feared, side effect is osteonecrosis of the jaw (ONJ); risk of this can be reduced by good oral hygiene and regular dental checks.

All patients will have an individual treatment plan throughout their life depending on the significance of their fracture risk, type of medication and intended lifestyle changes. The duration of the different therapies varies, and there is no uniform recommendation that applies to all patients. After a period of treatment, re-evaluation of the risk should be conducted, involving DXA, VFA (or X-ray of the spine) and fracture risk assessment.

Patients need to know from diagnosis that osteoporosis is a chronic condition, but that treatment duration is limited and periodical (the length of bisphosphonate treatment is 3–5 years). Good understanding of diagnosis and fracture risk is important because patients can then make informed choices regarding treatment and lifestyle changes. Low adherence and compliance are often low due to lack of knowledge, lack of guidance, invalid values and beliefs regarding therapies, side effects and the fact that patients do not directly ‘feel’ the benefits of the treatment, i.e. not having a fracture.

Nurses and other practitioners play a key role in improving compliance and adherence through specific nursing interventions including

  • Education about the treatment goal and benefits (this takes time)

  • Education about the prescribed drug regimen and recognising significant adverse reactions

  • Instructing the patient to report side effects

  • Advising patients on how to properly administer the medication

  • Assessing (and supporting) compliance and adherence

  • Informing and recording for how long patients must take their medication

  • Scheduling fracture risk re-evaluation

  • Advise on lifestyle modification regarding diet and exercise

  • Advise on good oral hygiene and regular dental care

  • Advise on prevention of falls (see Chap. 4)

  • Referring patients to national osteoporosis associations for support

2.5 The Role of Practitioners in Osteoporosis and Fracture Prevention, Case Finding, Risk Assessment, and Management and Education After Diagnosis

Nurses and other practitioners have significant roles in the multidisciplinary approach to diagnosis of osteoporosis. All those who provide care to older people and those who have already sustained a fragility fracture should be aware of the possibility of their patients having osteoporosis and an increased risk of further fracture. They must know how to assess and modify the risk factors, why and how osteoporosis is diagnosed and how to ensure that proper referrals are made. Nursing and care diagnoses that are appropriate for patients with osteoporosis include impaired mobility, deficient knowledge, imbalanced nutrition, risk for falls, risk for injury (if substantial bone loss is presently increasing the risk of fractures), and acute pain (if fractures occur due to bone loss).

People diagnosed with this chronic condition need support in developing coping strategies. Most newly diagnosed patients are afraid of sustaining another fracture and feel vulnerable, sometimes leading to a paralysing fear of falling. Patients with advanced osteoporosis often experience decreased ability to perform activities of daily living and suffer from chronic back pain. Depression, loss of self-esteem, disability and increasing physical dependence can be significant. Nurses and other practitioners can guide, advocate and educate as part of caregiving by helping patients to maintain function and improve quality of life [42] and can refer patients to national osteoporosis associations for further information and support.

The role of nurses and other practitioners in osteoporosis can be envisaged in the following different stages: case finding, risk assessment, and management and education after diagnosis. This can include the following tasks:

  • Incorporating simple questions on risk factors for osteoporosis into standard patient assessments and community questionnaires to improve early detection

  • Promoting education regarding bone health to prevent osteoporosis in general population, including children, young adults and parents

  • Providing education to other professional groups regarding bone health

  • Implementing screening programs in at-risk populations

  • Assessing the risk of falls in the elderly and promoting preventive strategies

  • Supporting individuals in the treatment and management of this condition through ongoing assessment, teaching and counselling after diagnosis

Further discussion of secondary fracture prevention services is considered in Chap. 5.

  • Promoting patients’ commitment and compliance to lifestyle modifications and treatment over the course of their lives, and to cope with chronic illness through the development of coping strategies and, as required, pain management

  • Providing ongoing remote telephone counselling and support

  • Promoting compliance and persistence with osteoporosis pharmacologic treatment drugs

2.6 Suggested Further Study

To effectively provide care to patients with or at risk of fragility factures, it is essential that the practitioners have extensive and up-to-date knowledge of osteoporosis and its prevention and management. Individual further study should be conducted using the strategies and resources to extend knowledge identified in Box 2.4.

Box 2.4 Strategies and Resources for Extending Knowledge About Osteoporosis and Fragility Fracture

  • Talk to patients and their family about the impact of sustaining a fragility fracture due to osteoporosis. Reflect on these conversations, and search for evidence-based literature to improve care and outcomes.

  • Expand knowledge by taking an online/e-learning course and use this to assess knowledge and performance yearly.

Online courses:

  • https://theros.org.uk/healthcare-professionals/courses-and-cpd/ Fracture Prevention Practitioner Training with the Royal Osteoporosis Society (UK): This is an interactive training course, which enables nurses with an interest in osteoporosis and fracture prevention to improve their knowledge and ability to deliver excellent health care to people with, or at risk of, osteoporosis and fragility fractures.

  • https://www.bonesource.org/ BoneSource™: This Professional Education Program from the Bone Health and Osteoporosis Foundation (USA) provides activities that are intended to improve the knowledge and competence for all healthcare professionals involved in the prevention, diagnosis and treatment of osteoporosis.

  • Read and make notes from books, articles and national or international guidelines on Osteoporosis and fracture prevention. The following are examples, but many other options exist:

Example websites:

International Osteoporosis Foundation www.capturethefracture.org/ and www.iofbonehealth.org

Fragility Fracture Network www.fragilityfracturenetwork.org/

Example books, articles and guidelines

Curtis, E.M. Moon, R.J. Harvey, N.C. Cooper, C. (2017) The impact of fragility fracture and approaches to osteoporosis risk assessment worldwide Bone. 104:29–38, 7–17 https://doi.org/10.1016/j.bone.2017.01.024

Falaschi, P. & Marsh, P. (Eds) (2021) Orthogeriatrics. The management of older patients with Fragility Fractures. Springer: Switzerland https://link.springer.com/book/10.1007/978-3-030-48126-1

Walsh J. S. (2017) Normal bone physiology, remodelling and its hormonal regulation, Surgery https://doi.org/10.1016/j.mpsur.2017.10.006

Guerado, E., Cano, J.R., Crespo, V., Campos, A. (2022). Bone Mineralization and Osteoporotic Changes. In: Pape, HC., Kates, S.L., Hierholzer, C., Bischoff-Ferrari, H.A. (eds) Senior Trauma Patients. Springer, Cham. https://doi.org/10.1007/978-3-030-91483-7_3

  • Meet with osteoporosis specialists to keep up to date on new developments and disseminate this knowledge to colleagues

2.7 How to Self-Assess Learning

  • Discuss within the local team if national guidelines for osteoporosis treatment and prevention and fragility fracture prevention are implemented correctly or need to be developed locally nationally.

  • Conduct peer review sessions within the team identifying how team performance impacts patient outcomes and develop action plans for how practice can be improved.

  • Undertake assessments contained within online courses listed above.