Week 12: Alterations of Musculoskeletal Function Flashcards
What is Osteoporosis?
Osteoporosis, or porous bone, is characterized by low bone mineral density caused by altered bone microstructure and leads to an increased risk of fractures. It is a complex, multifactorial, chronic disease that often progresses silently causing impaired structural integrity of the bone, and decreased bone strength. Simply stated, bone resorption outpaces bone deposition and clients develop weak bones. A progressive loss of bone mass may continue until the skeleton is no longer strong enough to support itself. Eventually, bones can fracture spontaneously. As bone becomes more fragile, fractures occur from falls or bumps that would not previously have caused fracture.
Types of osteoporosis include:
* Perimenopausal
* Iatrogenic
* Regional: osteoporosis is confined to a region or segment of the appendicular skeleton and usually has a known cause
* Postmenopausal
* Glucocorticoid-induced
* Age-related
What is Osteoarthritis?
Osteoarthritis (OA) is a degenerative, age-onset disease characterized by the wearing away of cartilage at articular joint surfaces. Weight-bearing joints such as the knee, vertebral column, and hip are most commonly affected. The hands are also affected because they are frequently used. OA seems affected by gender; the hands and knees are more commonly affected in females whereas the hips are more affected in men. Advancing disease reveals narrowing of the joint space because of cartilage loss, bone spurs (osteophytes), and often changes in the subchondral bone.
Identify the modifiable and non-modifiable risk factors in the development of fractures
Fracture incidence varies depending on bone involved, age, and gender. The highest incidence of fractures occurs in young males aged 15-24 and in adults 65 years and older. Rates of hip and wrist fractures tend to be higher in females.
Pediatric population:
* bone mineral content, bone size, bone accrual lower resulting in low bone mineral density
* genetic factors
* poor nutrition (i.e., inadequate intake of dietary calcium or excessive intake of carbonated beverages)
* lack of weight-bearing physical activity
* obesity
* play and sport (i.e., exposure to trauma)
Older adults:
* age
* gender (i.e., osteoperosis)
* smoking - impact on hormones
* alcohol - influence on bone structure and mass
* steroids - bone loss
* diabetes
* previous fracture
Identify the modifiable and non-modifiable risk factors in the development of osteoporosis
Genetic:
* family history of osteoporosis
* White or Asian race
* Increased age
* Female gender
Anthropometric:
* Small stature
* Fair or pale skinned
* Thin build
Hormonal and Metabolic:
* Early menopause
* Late manarche
* Nulliparity
* Obesity
* Hypogonadism
* Gaucher disease
* Cushing syndrome
* Weight below healthy range
* Acidosis
Dietary:
* Low dietary calcium and vitamin D
* Low endogenous magnesium
* Excessive protein
* Excessive sodium intake
* High caffeine intake
* Anorexia nervosa
* Malabsorption
Lifestyle:
* Sedentary
* Smoking
* Alcohol consumption (excessive)
Concurrent:
* Hyperparathyroidism
Illness & Trauma:
* Renal insufficiency, hypocalcemia
* Rheumatoid arthritis
* Spinal cord injury
* Systemic lupus erythematosus
Liver disease:
* Marrow disease
Drugs:
* Corticosteroids
* Dilantin
* Gonadotropin-releasing hormone agonists
* Loop diuretics
* Methotrexate
* Thyroid
* Heparin
* Cyclosporine
* Depo-medroxyprogesterone acetate
* Retinoids
Remember! CALCIUM
C: calcium & vitamin D intake low
A: age (after age 30 clast activity > blast activity, testosterone and estrogen drop)
L: lifestyle (i.e., smoking, exercise, etc.)
C: Caucasian or Asian, women
I: inherited
U: underweight
Medications: glucocorticoids, anticonvulsants, etc.
Identify the modifiable and non-modifiable risk factors in the development of osteoarthritis
The incidence of OA increases with age and is more common in females than in men older than age 50. The prevalence in individuals younger than age 45 is uncommon and generally does not exceed 20% in the elderly. Certain medications can stimulate collagen-digesting enzyme activity in the synovial membrane (e.g., colchicine, indomethacin, and steroids). With these conditions, the disease is noted as secondary osteoarthritis. Abnormal knee alignment also has been shown to increase the incidence and progression of OA. Both varus or valgus disorders of the knee of more than 5 degrees have been associated with increased risk of development and progression of OA. Although the use of biomechanical devices, such as foot wedges or alignment braces, has been shown to decrease pain, the reduction of disease progression has yet to be supported.
Explain the etiology of osteoarthritis
Currently, there is no single specific cause of OA; historically it has been viewed as a mechanical problem and emerging is the evidence of molecular events interacting with mechanical issues.OA may be classified as idiopathic or secondary. Idiopathic OA, the most common type, has no known cause but is associated with increasing age. The causes of secondary OA include trauma, mechanical stress, inflammation of the joint structures, neurological disorders, use of certain medications, and joint instability. Excessive weight contributes to the development of OA, particularly in the knee and hip. Other risk factors associated with OA include decreased estrogen in menopausal females, excessive growth hormone, and increased PTH.
OA has been commonly classified as noninflammatory joint disease. However, more recent discoveries have identified the presence of numerous cytokines, chemokines, prostaglandins, and apoptotic molecules within the disease process. The ensuing low-grade inflammation, calcification of articular cartilage, and interaction between transcription factors, cytokines, growth factors, matrix molecules, and enzymes affect development and progression of OA. This chemical cascade outlines how the process of cartilaginous destruction begins long before osteoarthritic changes can be detected through the use of MRI, arthroscopy, or traditional x-ray films.
Advancing disease reveals narrowing of the joint space because of cartilage loss, bone spurs (osteophytes), and often changes in the subchondral bone.
Explain the etiology & pathophysiology of fractures
Fractures occur when force applied exceeds the tensile or compressive strength of bone, resulting in a break in the continuity of a bone. Fractures are most commonly caused by falls, car accidents, and athletic injuries.
When a bone is broken the periosteum and blood vessels in the cortex, marrow, and surrounding soft tissues are disrupted. Bleeding occurs from the damaged ends of the bone and from the neighboring soft tissue. A hematoma forms within the medullary canal, between the fractured ends of the bone, and beneath the periosteum. Bone tissue immediately adjacent to the fracture dies. This necrotic tissue and any debris in the fracture area stimulate an intense inflammatory response characterized by vasodilation, exudation of plasma and leukocytes, and infiltration by inflammatory leukocytes and mast cells. Cytokines, including transforming growth factor-beta (TGF-B), platelet derived growth factor, prostaglandins, and other factors that promote healing, are released. Within 48 hours after the injury, vascular tissue invades the fracture area from the surrounding soft tissue and marrow cavity, and blood flow to the entire bone is increased. Osteoblasts and osteoclasts (or bone-forming cells) in the periosteum, endosteum, and marrow are activated to produce subperiosteal procallus along the outer surface of the shaft and over the broken ends of the bone.
Explain the etiology of osteoporosis
There are two types of osteoporosis: primary or idiopathic osteoporosis, which is the most common; and secondary osteoporosis. Secondary osteoporosis is caused by other conditions, including endocrine diseases (hormone imbalances, diabetes, hyperparathyroidism, hyperthyroidism), medications (such as heparin, corticosteroids, phenytoin, barbiturates, lithium), and other substances (including tobacco and ethanol). Other conditions (including rheumatoid disease, human immunodeficiency virus [HIV], malignancies, malabsorption syndromes, liver or kidney disease) also increase the risk for developing osteoporosis. Primary Osteoporosis is associated with the process of normal aging. Age-related bone loss begins in the third to fourth decade. The cause remains unclear, but it is known that decreased serum growth hormone (GH) and IGF levels along with increased binding of RANKL and decreased OPG affect osteoblast and osteoclast function. Secondary osteoporosis sometimes develops temporarily in individuals receiving large doses of heparin, perhaps because heparin promotes bone resorption by decreasing collagen synthesis or by increasing collagen breakdown. Osteoporosis caused by heparin therapy usually resolves when therapy ceases. Treatment with other medications may lead to the development of osteoporosis, such as the use of glucocorticoid treatment for many chronic disease processes. Other medications that increase the risk of osteoporosis include lithium, methotrexate, anticonvulsants, cyclophosphamide, and cyclosporine. One secondary cause, transient osteoporosis of the hip, is associated with the third trimester of pregnancy or the immediate postpartum period. However, most transient osteoporosis is a typically self-limiting syndrome affecting the lower extremity joints of middle-aged men. The etiology is unknown, and although most cases spontaneously resolve, some occurrences of bone demineralization may be related to osteonecrosis. Postmenopausal osteoporosis is characterized by increased bone resorption relative to the rate of bone formation, leading to sustained bone loss resulting from estrogen deficiency. Bone loss resulting from estrogen deficiency also contributes to osteoporosis in men.
Discuss the diagnostics for osteoarthritis
Evaluation consists of individual subjective reports, clinical assessment (including a detailed history and physical examination), and radiologic studies, which may include a CT scan, arthroscopy, and MRI, as well as tradition x-ray films.
The joints of a client with osteoarthritis are characteristically hard and cool to palpation. Radiologic hallmarks of primary osteoarthritis include:
* non-uniform joint space loss
* subchondral sclerosis
* cyst formation
* osteophyte formation (bone spurs)
Discuss the diagnostics for osteoporosis
Osteoporosis is asymptomatic unless fracture occurs, so often diagnosis is delayed. By the time abnormalities are detected by x-ray, 25-30% of bone may be gone. Measuring bone mineral density by using dual x-ray absorptiometry (DXA) continues to be the most common method of estimating bone mass. The WHO has also developed an assessment tool (FRAX) to estimate an individual’s 10-year risk of fracture. Bone quality related not just to bone mass (as measured by bone density) but also to the microarchitecture of the bone. Other variables include crystal size and shape, brittleness, vitality of the bone cells, structure of the bone proteins, water volume, integrity of the trabecular network, vascular supply, and the ability to repair tiny cracks. Other evaluation procedures include tests for levels of serum calcium, phosphorus, and alkaline phosphatase as well as protein electrophoresis.
According to the WHO:
1. normal bone mass is greater than 833 mg/cm2
2. Osteopenia, or decreased bone mass it 833-648 mg/cm2
3. Osteoporosis is bone mass less than 648 mg/cm2
Signs & Symptoms:
Remember FRAIL
F: fractures (hips, spine, and wrist)
R: rounding of upper back “Dowager’s hump”
A: asymptomatic
I: inches of height lost (approx. 2-3 inches)
L: lower back, neck, and hip pain
Discuss the diagnostics & treatment for fractures
Diagnostics are typically performed and confirmed by X-ray.
Treatment of a displaced fracture involves manipulating the bone to realign bone fragments (reduction) to the correct anatomic position and holding the fragments in place (immobilization) so bone healing can occur. Many fractures heal without manipulation and require only adequate immobilization. Several methods of manipulation are available to reduce a fracture that will not heal with simple immobilization, including closed manipulation, traction, and open reduction. Maligned fractures require the most aggressive treatment of all types of fractures.
Fractures can be reduced by closed manipulation if the skin is not opened and the bone is able to be moved or manipulated into place. Appropriate use of closed manipulation occurs when the contour of the bone is well aligned and the alignment can be maintained with immobilization.
Traction is another option used to accomplish or maintain reduction of a fracture. When bone fragments are displaced (not in their anatomic position), weights are used to apply firm, steady traction (pull) and countertraction to the long axis of the bone. Traction stretches and fatigues muscles that pull the bone fragments out of place, allowing the distal fragment to align with the proximal fragment. Traction can be applied to the skin (skin traction), directly to the involved bone, or distal to the involved bone (skeletal traction). Skin traction is used when only a few pounds of pulling force are needed to realign the fragments or when the traction will be used for only a brief time, such as before surgery or for a few days before applying a cast. In skeletal traction, a pin or wire is drilled through the bone below the fracture site, and a traction bow, rope, and weights are attached to the pin or wire to apply tension by providing the pulling force needed to overcome the muscle spasm and helping realign the fracture fragments.
Open reduction is a surgical procedure that exposes the fracture site; the fragments are brought into alignment under direct visualization. Some form of hardware, such as a screw, plate, nail, or wire, is used to maintain the reduction (internal fixation). External fixation is a procedure used to reduce and immobilize significantly displaced open fractures. Pins are placed in the bone proximal and distal to the break and then stabilized by an external frame of clamps and rods. Bone grafts also are used to repair fractures and filling voids in the bone. These grafts are from the injured individual (autograph), a cadaver (allograft), or a bone substitute (ceramic composites, bioactive cement).
Treatment of delayed union and nonunion fractures includes use of various modalities designed to stimulate new bone formation. Physical modalities, such as implantable or external electric current devices, electromagnetic field generations, and low-density ultrasound, have been effective in stimulating bone formation. Stem cells and gene therapy also show promise in promoting formation of new bone. Large defects in bone can be filled with bone graft or synthetic materials, such as calcium phosphate cement.
Discuss prevention and treatment requirements for osteoporosis
Regular, moderate weightbearing exercise can slow the rate of bone loss and, in some cases, reverse demineralization because the mechanical stress of exercise stimulates bone formation. It is important to reduce the risk of falls and enhance bone quality. Therefore, an exercise program to enhance muscle strength is advised.
Important new findings suggest that estrogen may prevent excessive bone loss before and after menopause by limiting osteoclast life span through promotion of apoptosis. Calcium intake sufficient to maintain normal calcium balance during adolescence and sufficient intake of magnesium is also helpful in prevention. Treatment includes the use of bisphosphonates, estrogen, and diet.
The role of calcium intake to prevent and treat osteoporosis is controversial (can cause renal stones with little evidence in improving BMD). It is well accepted that oral calcium intake sufficient to maintain normal calcium balance is necessary during adolescence to ensure development of peak bone mass, and that calcium-deficient diets can aggravate bone loss associated with menopause and aging. Although recommendations have been established for young females of 1000 mg of calcium daily (particularly from dietary sources) and for postmenopausal females of 1500 mg daily (with vitamin D), it has been difficult to translate these recommendations into clear-cut clinical outcomes. A significant relationship has been observed between an individual’s lifetime history of calcium intake and peak bone mineral density. Diets with higher fruit and vegetable intake seem to correlate with higher BMD. Other nutrients that appear to have a positive impact on bone health include magnesium, vitamin K2, and docosahexaenoic acid or DHA. Magnesium (Mg++), another mineral important for skeletal development, is an essential mineral in many biochemical and physiologic functions, including activation of enzymes, involvement in adenosine triphosphate (ATP) synthesis and protein synthesis, regulation of membrane channels, and contraction of muscle. Mg++ is important to bone quality because it helps control hydroxyapatite crystal growth and thereby prevents formation of brittle bones. It seems reasonable that Mg++ is required for normal calcium (Ca++) absorption because severe Mg++ deficiency results in hypocalcemia.
Discuss dietary requirements and treatment for osteoarthritis
Treatment of osteoarthritis is determined by the severity of pain and immobility. Pharmacologic therapy may include the use of analgesics and anti-inflammatory drug therapies, such as intra-articular corticosteroids and hyaluronate sodium (like the hyaluronic acid we put on our skin! Is a humectant and draws water in). Sodium hyaluronate acts like the synovial fluid in the joint, preventing friction and further inflammation but sort of “cushioning” the joints. The combination of MSM, glucosamine, and chondroitin may be effective, as may topical drugs such as capsaicin cream and balms (derived from peppers - spicy).
Non-pharmacological therapies are also an essential component of OA management. Walking, non-impact aerobics, and passive range-of-motion exercises are important to maintain joint flexibility. Improving muscle strength, especially of the quadriceps muscle, will help clients to improve their ability to perform activities of daily living. Bracing may help to keep joints positioned correctly and to relieve pain. Knowledge of proper body mechanics and posture may offer some benefit. Clients who are obese should consider a weight loss program, especially if weight-bearing joints such as the hip and knee are affected. Weight loss has been associated with decreased pain and disability. Surgical procedures such as joint replacement and reconstructive surgery may become necessary when other methods are ineffective. Complementary therapies such as the use of magnetic bracelets, therapeutic ultrasound, and acupuncture may also be helpful.
Dietary requirements include increasing the intake of Omega-3 fatty acids, ensuring safe sun exposure, and eating food sources rich in Vitamins D and K.
What are osteocytes?
(Bone Cells) The most abundant cells in bone, are transformed osteoblasts trapped or surrounded in osteoid as it hardens because of minerals that enter during calcification. It is the final differentiation stage for an osteoblast. The osteocyte is within a space in the hardened bone matrix called a lacuna. Osteocytes have numerous functions, including acting as mechanoreceptors and synthesizing certain matrix molecules, playing a major role in controlling osteoblast differentiation and production of growth factors, and maintaining bone homeostasis.
What is the difference between osteoblasts and osteoclasts?
(Bone breakdown - resorption) Osteoclasts are the major resorptive cells of bone. They migrate over bone surfaces to resorption areas that have been prepared and stripped of osteoid by enzymes, such as collagenases produced by osteoblasts in the presence of PTH, which is necessary for the resorptive process.
(Bone formation - deposition) Osteoblasts, originating from MSCs, osteoblasts are the primary bone-producing cells and are involved in many functions related to the skeletal system. Mature osteoblasts produce inorganic calcium phosphate, which is converted to hydroxyapatite, and an organic matrix that is composed mainly of type I collagen. Once this process is complete, osteoblasts deposit new bone in response to the bone resorbed by osteoclasts.
Discuss fracture classifications
Complete: the integrity of the bone is broken into two pieces
Incomplete: the bone is damaged but still in one piece
Open: formerly referred to as a compound fracture, is characterized by a concurrent break in the skin in the area of the fracture
Closed: formerly referred to as a simple fracture, has no break in the surrounding skin
Linear: fracture runs parallel to the long axis of the bone
Oblique: fracture is a slanted fracture of the shaft of the bone
Spiral: encircles the bone
Transverse: occurs straight across the bone
Comminuted: a bone breaks in two or more fragments
What are the three main types of incomplete fractures?
Greenstick, buckle or torus, and bowing. A greenstick fracture perforates one cortex and splinters the spongy bone and is relatively unstable. In a buckle or torus fracture, the cortex of the bone buckles but does not break, thus making it a relatively stable fracture. Bowing fractures usually occur when longitudinal force is applied to bone. This type of fracture is common in children. A complete diaphyseal fracture occurs in one bone of the pair, which disperses the stress sufficiently to prevent a complete fracture of the second bone, which bows. Treatment of a bowing fracture is difficult because the bowed bone interferes with the reduction of the fractured bone. In addition, a bowing fracture resists correction (reduction) because the force necessary to reduce it must be equal to the force that caused the initial injury. A fracture that results from a trauma that would not normally cause a fracture (a low-level trauma) is termed a fragility fracture. Fragility fractures are often a sequela of osteoporosis. A pathologic fracture is a break at the site of a preexisting abnormality (such as a tumor), usually by force that would not fracture a healthy bone. Any disease process that weakens a bone (especially the cortex) predisposes the bone to pathologic fracture. This type of fracture is most commonly associated with tumors, infections, osteoporosis, and other metabolic bone disorders.
Discuss the healing process of fractures
Bone is unique, after a fracture, it will heal with normal tissue - not scar tissue! Healing generally occurs in three overlapping phases, starting with the inflammatory phase that lasts 3-4 day. During the inflammatory phase, bone tissue destruction triggers and inflammatory response and hematoma formation. Following the inflammatory phase, the repair phase begins and capillary ingrowth, together with mononuclear cells and fibroblasts, begin the transformation of a hematoma into granulation tissue. Next, osteoblasts within the pro-callus synthesize collagen and matrix, which becomes mineralized to form callus. This phase can last several days. As the repair process continues, remodeling occurs, during which unnecessary callus is resorbed and trabeculae are formed along lines of stress. At the end of this stage, bone can withstand normal stresses. This phase can last months to years.
Discuss the manifestations of fractures
Clinical manifestations of a fracture can vary according to the type of fracture, site, and associated soft tissue injury. In general, the signs and symptoms of a fracture include impaired function, unnatural alignment (deformity), swelling, muscle spasm, tenderness, pain and impaired sensation. The position of the bone segments is determined by the pull of attached muscles, gravity, and the direction and magnitude of the force that caused the fracture. One or both segments of the fractured bone may be rotated inward or outward on the bone’s long axis (rotation), misaligned at an angle (angulation), or slide over the other segment (overriding) or out of normal position (displaced).
Discuss complications of fractures
Improper reduction or immobilization of a fractured bone may result in nonunion, delayed union, or malunion. Nonunion is failure of the bone ends to grow together. The gap between the broken ends of the bone fills with dense fibrous and fibrocartilaginous tissue instead of new bone. Occasionally, the fibrous tissue contains a fluid-filled space that resembles a joint, termed a false joint, or pseudarthrosis. Delayed union is union that does not occur until approximately 8 to 9 months after a fracture. Malunion is the healing of a bone in a nonanatomic position. Treatment of delayed union and nonunion includes use of various modalities designed to stimulate new bone formation. Physical modalities, such as implantable or external electric current devices, electromagnetic field generations, and low-density ultrasound, have been effective in stimulating bone formation. Stem cells and gene therapy also show promise in promoting formation of new bone. Large defects in bone can be filled with bone graft or synthetic materials, such as calcium phosphate cement. Broken bone can also damage surrounding tissue, periosteum, and blood vessels in cortex and marrow.
Dislocation is the temporary displacement of a bone from its normal position in a joint. If a dislocation does not involve a fracture, it is a simple dislocation; if there is an associated fracture, it becomes a complex dislocation. If the contact between the two joint surfaces is only partially lost, the injury is called a subluxation.
Dislocation and subluxation are most common in persons younger than 20 years and are generally associated with fractures.
Pediatric complications:
* growth plates vulnerable to fracture
* can result in shorter or crooked limb
* children’s bones heal faster, need to be seen more quickly - especially if manipulation of bone is required
Older adults:
* increased mortality, pain, disability, depression, and loss of independence
* high risk of morbidity and mortality after osteoporotic fracture
Discuss the pathophysiology of osteoporosis
Osteoporosis develops when the remodeling cycle - the process of bone resorption and bone formation - is disrupted and bone demineralization leads to decreased bone density (porous bones). The most common risk factor associated with the development
of osteoporosis is the onset of menopause. When females reach menopause, estrogen secretion declines and bones become weak and fragile. One theory to explain this occurrence is that normal levels of estrogen may limit the lifespan of osteoclasts, the bone cells that resorb bone. When estrogen levels decrease, osteoclast activity is no longer controlled, and bone demineralization is accelerated, resulting in loss of bone density. In females with osteoporosis, fractures often occur in the hips, wrists, forearms, or spine.
Although hormonal influences remain important in maintaining bone health, genetic factors and the role of oxidative stress are receiving increased attention as critical determinants of bone homeostasis. Reactive oxygen species (ROSs) are normal byproducts of aerobic metabolism, and although they can cause cell damage, at levels below which they cause oxidative stress (OS), ROSs serve as signaling molecules for many cell types, including osteocytes, osteoblasts, and osteoclasts. When excess ROSs accumulate, OS occurs and can result in loss of bone mass and bone strength.
The osteoclast differentiation pathway is directed by a series of processes that include proliferation, differentiation, fusion, and activation. These processes are controlled by hormones, cytokines, and paracrine stromal-cell microenvironment interactions. Thus, the intercellular communication in bone and the key molecular regulators are necessary for bone homeostasis. Certain transcription factors, known as Forkhead box (FoxO), help protect against the effects of OS by preventing excess accumulation of ROS and regulating certain genes that affect DNA repair and cell life span. FoxOs help remove damaged and abnormal cells by inducing apoptosis.
Interleukins (IL-1, IL-4, IL-6, IL-7, IL-11, IL-17), tumor necrosis factor-alpha (TNF-α), transforming growth factor-beta (TGF-β), prostaglandin E2, and hormones interact to control osteoclasts. Normal bone homeostasis is dependent on the balance between the cytokine receptor activator of nuclear factor κβ ligand (RANKL), its receptor RANK, and its decoy receptor osteoprotegerin (OPG); understanding this has led to a tremendously increased knowledge of osteoclast biology and pathogenesis of bone loss.
Discuss the OPG/RANKL/RANK System in osteoporosis
RANKL is a cytokine that activates the receptor RANK on osteoclast precursor cells and mature osteoclasts to activate intracellular signaling pathways that promote osteoclast activity and bone resorption and eventually bone loss. OPG is a glycoprotein that acts as an antagonist (decoy receptor) for RANKL. Essentially, it takes RANKLs’ spot and prevents it from binding and activating RANK. In this way, OPG helps to regulate bone resorption. In osteoporosis, this system is dysregulated. Specifically, estrogen plays a large role in the secretion of OPG, which is why declining estrogen is a problem in osteoporosis.
In the immune system, RANKL is expressed and secreted by T cells. T-cell derived RANKL can also activate RANK in osteoclasts, T cells, and dendritic cells, which enhances bone loss that occurs in inflammatory bone diseases such as rheumatoid arthritis.
In the vascular system, endothelial cells express RANKL and the RANK receptor.
Describe the manifestations of osteoporosis
The specific clinical manifestations of osteoporosis depend on the bones involved. The most common manifestation, however, is bone deformity. Pain tends to occur only when there is a fragility fracture. Fractures are likely to occur because the trabeculae of spongy bone become thin and sparse and compact bone becomes porous. As the bones lose volume, they become brittle and weak and may collapse or become misshapen. Vertebral collapse causes kyphosis (hunchback) and diminished height. Fractures of the long bones (particularly the femur and humerus), distal radius, ribs, and vertebrae are most common. The most serious fractures associated with osteoporosis are hip fractures because of their resultant chronic pain, disability, diminished quality of life, and premature death. Fracture of the neck of the femur (intertrochanteric fracture) tends to occur in older adult females with osteoporosis. Cortical bone becomes more porous and thinner, making bone weaker and prone to fractures. Loss of trabecular bone in men proceeds in a linear fashion, with thinning of trabecular bone rather than complete loss as is noted in females.
Fatal complications of osteoporotic fractures include:
* fat or pulmonary embolisms
* hemorrhage
* shock
