Muscles
Sarcopenia, drug-induced myopathies (statins.), necrosis (diabetes mellitus), fat atrophy (steroids)
Tendons
Chondrocalcinosis, hypercholesterolemia, hyperuricemia, hypervitaminosis A, drug-induced (quinolones)
Cartilage
Chondrocalcinosis, hyperuricemia, recurrent haemorrhage, hemochromatosis, ochronosis
Synovium
Hyperuricemia, amyloidosis
Bone
Osteopenia, osteoporosis, rickets, osteomalacia, renal osteodystrophy, hyperparathyroidism, thyroid acropachy, acromegaly, drug-induced disorders
Bone marrow
Hemosiderosis, aplasia, anemias, serous atrophy, fatty atrophy, drug-induced disorders
Normal Bone Metabolism
Bone is a specialized connective tissue made up of a matrix of collagen fibers, mucopolysaccharides and inorganic crystalline mineral matrix (calcium hydroxyapatite) that is distributed along the length of the collagen fibers. Bone remains metabolically active throughout life (bone turnover) with bone being constantly resorbed by osteoclasts (osteoclastic activity) and accreted by osteoblasts (osteoblastic activity) [1, 2]. Since bone turnover mainly takes place on bone surface, trabecular bone which has a greater surface to volume ratio than compact bone, is consequently some eight times more metabolically active than cortical bone. The strength of bone is related not only to its hardness and other physical properties but also to its size, shape, and architectural arrangement of the compact and trabecular bone.
Bone formation and bone resorption are linked in a consistent sequence under normal circumstances. Percursor bone cells are activated at a particular skeletal site to form osteoclast, which erode a flairly constant amount of bone. After a period of time, the bone resorption ceases and osteoblasts are required to fill the eroded space with new bone tissue. This coupling of osteoblastic and osteoclastic activity constitutes the basal multi-cellular unit (BMU) of bone and is normally in balance, with the amount of bone eroded being replaced with amount of new bone in about 3–4 months. At any one time, there are numerous BMUs throughout the skeleton at different stages of this cycle. The amount of bone in the skeleton at any moment is entirely dependent on peak bone mass attained during puberty and adolescence and on the balance between bone resorption and formation. Bone turnover is under the influence of general factors including age and hormones but is also locally modified by many factors such as physical forces.
Osteoporosis
Definition
Osteoporosis, by far the most common metabolic disease in western countries, is a systemic skeletal disease with quantitative abnormality of bone whereas, in rickets/osteomalacia, there is qualitative abnormality of bone (Fig. 1). Osteoporosis is characterized by reduction in bone mass (amount of mineralized bone per volume unit) and by altered trabecular structure due to a loss of trabeculae interconnectivity with a consequent increase in bone fragility (decrease in biomechanical strength) and susceptibility to fracture (insufficiency fractures) [3] (Fig. 2).
Fig. 1
Osteopenia and osteomalacia. (a) Osteopenia is characterized by quantitative bone abnormality with decreased bone density and cortical thinning (arrows). (b) Osteomalacia is characterized by qualitative bone abnormality with intracortical lucencies (arrows)
Fig. 2
Osteoporosis. Presence of multiple vertebral fractures with thoracic kyphosis. Sclerosis in fractured vertebral bodies corresponds to bone callus. Note the sternal fracture associated with thoracic kyphosis
Prevalence of Osteoporosis
In the western world, osteoporosis is reported to affect 1 in 2 women and 1 in 5 men older than the age of 50 years in their life time [4]. The risk of fracture increases with advancing age and progressive loss of bone mass and varies with the population being considered. The incidence of hip fracture has doubled over the past three decades and is predicted to continue to grow beyond what one would predicted from increased longevity. At 1 year after hip fracture, 40% patients are unable to walk independently, 60% have difficulty with one essential activity of life, 80% are restricted in other leaving activity, and 27% will be admitted to a nursing home for the first time [4].
Clinical Presentation and Etiology
Generalized osteoporosis is the end-stage of several diseases and can be either primary or secondary (Tables 2 and 3). Clinical significance of osteoporosis is limited until fractures develop. Vertebral fractures are the most commonly occurring osteoporotic fractures (Fig. 2). They occur as an acute event related to minor trauma or spontaneously. Vertebral fractures cause disability and limited spinal mobility and are associated within increased morbidity but symptoms generally resolve spontaneously over 6–8 weeks. They are powerful predictors of future fracture with a 12% increased risk of a future vertebral fracture within 12 months if a single vertebral fracture is present (22% increased risk in the presence of multiple fractures) [2]. Questionnaires are also available to evaluate fracture risk (FRAX). Consequently, the accurate identification and clear reporting of vertebral fracture by radiologists have a vital role to play in the diagnosis and appropriate management of patient with, or at risk of, osteoporosis.
Table 2
Causes of primary osteoporosis
Idiopathic juvenile osteoporosis: self-limited (2–4 year duration) form of osteoporosis in pre-pubertal children. Acute course of the disease with growth arrest and fractures. Mild to severe forms. Differential diagnosis: osteogenesis perfecta or other forms of juvenile osteoporosis. Cortisolism and leukaemia |
Post-monopausal (type I) osteoporosis: Onset at the time of menopause but important bone loss during first 4 years after the menopause related to reduction in blood oestrogen. Clinically significant in women 15–20 years after the menopause. Fractures in bones with high trabecular cortical ratio (vertebral bodies and distal forearm) |
Senile (type 2) osteoporosis: men and women 75 years or older due to age-related bone loss (age-related impaired bone formation associated with secondary hyperparathyroidism as a consequence of reduced calcium absorption from the intestine secondary to decreased production of the active metabolic vitamine D in the kidney). Reduction in both cortical and trabecular bone. Fractures in vertebrae but also in bones with low trabecular cortical ratio (tibia, humerus and pelvis) |
Osteogenesis imperfecta: congenital disorders due to gene mutation associated with osteoporosis of variable severity. Blue sclerae and occasional dental involvement |
Table 3
Causes of secondary osteoporosis
Endocrine: glucocorticoid excess, oestrogene/testosterone deficiency, hyperthyroidism, hyperparathyroidism |
Nutritional: intestinal malabsorption, chronic alcoholism, chronic liver disease, partial gastrectomy, vitamine C deficiency |
Hereditary: homocystineuria, Marfan syndrome, Heler-Danlos syndrome |
Hematologic: sickle-cell disease, thalassemia, Gaucher disease, multiple myeloma |
Others: rheumatoid arthritis, hemochromatosis, long-term heparin therapy |
Imaging Findings in Osteoporosis
Radiography is relatively insensitive in detecting early bone loss and 30–40% loss of bone tissue usually remain occult on radiographs. Radiographic bone density is also affected by patient characteristics and technical parameters used to obtain the radiographs. The subjectivity of visual judgement of bone density on conventional radiographs supports the value of modern quantitative techniques such as bone densitometry.
The main radiographic features of generalized osteoporosis include cortical thinning and disappearance of the trabecular network. Resorption and thinning of trabeculae initially affect secondary trabeculae that are parallel to the biomechanical stresses and the primary trabeculae that are perpendicular to the biomechanical stresses may appear more prominent because they are affected at a later stage (Fig. 3).
Fig. 3
Osteoporosis and vertebral fracture. (a) A sagittal CT reformat of the thoracic spine shows reduced trabecular bone density and a vertebral fracture. (b) The corresponding sagittal T1-w SE image shows decreased signal intensity in the fractured vertebral body (recent fracture). Altered trabecular bone pattern seen on CT is not visible on routine MR images
Cortical thinning occurs as a result of endosteal, periosteal, or intra-cortical (cortical tunnelling) bone resorption. Endosteal resorption is the least specific radiographic finding because it may be evident in metabolic disorders, including osteoporosis but also in marrow disorders. Intra-cortical tunnelling is more specific occurring mainly in disorders with rapid bone turnover such as diffuse osteoporosis and reflex sympathetic osteodystrophy. Subperiosteal resorption is the most specific finding, being diagnostic of hyperparathyroidism.
Osteoporosis remains occult on MR images (Fig. 3) although a relationship between trabecular bone density and marrow fat has been reported. The presence at spine MRI of multiple vertebral fractures including acute (marrow edema) and healed (marrow fat) fractures suggests increased bone fragility and, hence, osteoporosis.
Quantification of Osteoporosis
Several quantitative techniques including Dual energy X-ray absorptiometry (DXA), quantitative computed tomography (QCT), and quantitative ultrasonography (QUS) have been developed to enable accurate and precise assessment of mineral bone density [2]. Several methods have been used in the past to standardize measurements of cortical thickness (radiogrametry), trabecular pattern (Singh index), and vertebral deformity (morphometry) from radiographs (Table 4). These measurements lack accuracy or predictive value but they remain worth reporting when present on radiographs.
Table 4
Radiographic quantitative methods for osteoporosis
Radiogrametry involves the measurement of cortical thickness of various bones on radiographs and the most frequently used bone is the second metacarpal bone of the non dominant hand. The metacarpal index corresponds to the ratio between the mid diaphyseal diameter of the bone (from each periosteal surface) and the medullary cavity (distance between endosteal surface) |
Trabecular pattern was assessed by using the Singh index which takes into account the number, thickness and arrangement of trabeculae in the femoral neck. Texture analysis of that area could be of interest |
Vertebral morphometry according to various methods have been proposed to standardize a subjective visual assessment vertebral fracture and to quantitate alteration in vertebral height and shape. Vertebral fractures are defined as endplate, wedge or crush. Changes in shape of the vertebrae are generally defined by the six points methods, in which the anterior, mid- and posterior points of the superior and inferior endplates of the vertebral body are identified, to measure anterior, mid, and posterior height. The change in shape can be graded (mild, moderate, severe) for each pattern on deformity (wedge, biconcave, crush) |
Rickets and Osteomalacia
Rickets and osteomalacia are similar metabolic bone disorders characterized by inadequate or delayed mineralization of osteoid in cortical and trabecular bone in children and in adults, respectively [5].
Pseudofracture or looser’s zone is the radiological hallmark of osteomalacia as it represents cortical fracture without a mineralized callus. Looser’s zone corresponds to a linear cortical lucency frequently perpendicular to the cortex of the bone without periosteal reaction (Fig. 4). It typically involves the ribs, the superior and inferior pubic rami, and the inner margins of the proximal femora or lateral margin of the scapula. Widened physeal growth plate and metaphyseal cupping and fraying are the radiological signs of rickets that are best seen at rapidly growing ends of bone such as distal femur and radius or anterior ends of ribs. Additional radiological findings of rickets/osteomalacia include bone deformities, osteopenia or a coarsened pattern of the cancellous bone [5].
Fig. 4
Osteomalacia. (a) A lateral radiograph of a femur from a patient with osteomalacia demonstrates anterior bowing of the femoral shaft and a lucent line corresponding to a fracture (white arrow). (b) A close–up radiograph of a femoral neck in another patient with osteomalacia demonstrates cortical discontinuity and bone resorption (black arrow) corresponding to a chronic fracture or Looser’s zone
There is no hallmark of osteomalacia at MR imaging because cortical fractures with deficient healing (Looser’s zones) are difficult to detect on MR images. However, the presence of multiple trabecular bone fractures with variable appearance on fluid-sensitive sequences should suggest osteomalacia. This variability could reflect the deficient healing process associated with osteomalacia [6, 7] (Fig. 5).
Fig. 5
Osteomalacia. (a, b) Coronal T1-weighted images of the pelvis of a patient with osteomalacia demonstrate multiple trabecular bone fractures (arrows)
Renal Osteodystrophy and Hyperparathyroidism
The term renal osteodystrophy relates to all musculoskeletal manifestations of chronic renal failure [5]. Traditionally, renal osteodystrophy encompassed osteoporosis, osteomalacia, secondary hyperparathyroidism and soft tissue calcifications. The radiographic signs of hyperparathyroidism are subperiosteal bone resorption on the radial side of the finger phalanges and/or exclusive phalangeal tuft resorption (Fig. 6). The hand is the earliest and most sensitive site for detection of hyperparathyroidism but bone resorption can also be seen at the end of the clavicle, at the sacro-iliac joints or on periosteal surfaces of the proximal humeri or proximal femora. Marginal erosions in small joints can also develop most likely due to traction at capsular insertions. They are usually discrete and joint space is preserved.
Fig. 6
Hyperparathyroidism. (a) Radiographic signs of hyperparathyroidism include subperiosteal bone and phalangeal tuft resorption. (b) After successful treatment, reappearance of woven bone
Osteosclerosis may also be encountered in renal osteodystrophy. It is commonly appreciated in vertebrae, pelvis, ribs and metaphyses of long tubular bones. In vertebrae, sclerosis is frequently confined to the end-plates, producing a characteristic appearance of alternating bands of different density (the “rugger jersey” spine).