Ebook Imaging of bones and joints: Part 2
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Ebook Imaging of bones and joints: Part 2
6 Osteonecroses of the Skeletal System6.1 Anatomy, Etiology, and Pathogenesis► Anatomy. Bone varies significantly in its composition, depending on age Ebook Imaging of bones and joints: Part 2e and location. It has an organic matrix, comprised of primarily collagen (osteoid), into which inorganic mineral components (especially calcium hydroxyapatite) are incorporated. The mineralized matrix is subject to constant resorption and formation by specific cells (osteoblasts and osteoclasts). T Ebook Imaging of bones and joints: Part 2his matrix harbors both red (hematopoietic) and yellow (fatty) marrow. These are the components that, together with the mineralized bony matrix, constEbook Imaging of bones and joints: Part 2
itute the organ “bone.” Survival of the bone is not possible, however, without arterial inflow and venous drainage.For purposes of clarification. Oste6 Osteonecroses of the Skeletal System6.1 Anatomy, Etiology, and Pathogenesis► Anatomy. Bone varies significantly in its composition, depending on age Ebook Imaging of bones and joints: Part 2 involved where ischemia is present. Cellular death in bone is a nonspecific, commonly subclinical, process that occurs more often when bone cells are subjected to abnormal stress. Therefore, histopathology will reveal small areas of necrosis along with severe osteoarthritis, stress or insufficiency Ebook Imaging of bones and joints: Part 2 fracture, an acute fracture, tumor, or infection. This chapter addresses clinically relevant forms of osteonecrosis which can be readily demonstratedEbook Imaging of bones and joints: Part 2
by imaging studies. Imaging reflects macroscopic anatomy and reveals the effects of cell death on the bone (or parts of it). Common terms such as “os6 Osteonecroses of the Skeletal System6.1 Anatomy, Etiology, and Pathogenesis► Anatomy. Bone varies significantly in its composition, depending on age Ebook Imaging of bones and joints: Part 2ovide information about prognosis or etiology.In everyday language, the term "osteonecrosis" generally refers to bone necrosis located in the epiphysis or apophysis or involving the entire bone ( * Fig. W6.1). If the osteonecrosis Is located in the metaphysis or diaphysis, then this is referred to a Ebook Imaging of bones and joints: Part 2s "bone infarct." A task for the future is to devise a classification system for bone necrosis that provides prognostic information independent of theEbook Imaging of bones and joints: Part 2
skeletal location.►Etiology. In many cases the etiology and pathogenesis are obvious, such as interruption of blood supply secondary to a dislocation6 Osteonecroses of the Skeletal System6.1 Anatomy, Etiology, and Pathogenesis► Anatomy. Bone varies significantly in its composition, depending on age Ebook Imaging of bones and joints: Part 2t risk factors. Additionally, some genetic factors that may predispose to bone necrosis have been identified.Osteonecrosis without a clear etiology is referred to as “primary,’’“idiopathic,” or “spontaneous” osteonecrosis.►Pathology. A number of theories have been advanced to describe the processes Ebook Imaging of bones and joints: Part 2involved in the pathogenesis of osteonecrosis. It is generally accepted that all of them ultimately end in a reduced or interrupted supply of oxygenatEbook Imaging of bones and joints: Part 2
ed blood to the bone. Ischemia prevents the normal repair processes of microfractures; results in the death of osteocytes, fat cells, and cells of hem6 Osteonecroses of the Skeletal System6.1 Anatomy, Etiology, and Pathogenesis► Anatomy. Bone varies significantly in its composition, depending on age Ebook Imaging of bones and joints: Part 2s are activated to absorb dead trabeculae. Fibrovascular tissue is formed to enclose the dead bone. This tissue is partially converted to bone. If the zone of necrosis involves the metaphysis or diaphysis, it will have no biomechanical impact. The same holds true for small epiphyseal lesions. If a l Ebook Imaging of bones and joints: Part 2arger necrotic zone and/or a lesion located within a weight-bearing area of a joint is placed under significant stress, then disruption of bone architEbook Imaging of bones and joints: Part 2
ecture will lead to functional failure with subsequent subchondral fracture and collapse of the joint surface.Table 6.1 Risk factors for necrosis of t6 Osteonecroses of the Skeletal System6.1 Anatomy, Etiology, and Pathogenesis► Anatomy. Bone varies significantly in its composition, depending on age Ebook Imaging of bones and joints: Part 2sphonates •RadiotherapyNutritional• AlcoholHematologiconcologic•Previous renal transplant (even without steroids) •Hemoglobinopathies (sickle cell anemia, thalassemia) •LeukemiaMetabolic•Gaucher's disease •Pancreatitis with fat embolismRheum.itologiccd•Systemic lupus erythematosus •Nec rotizing arte Ebook Imaging of bones and joints: Part 2ritisInfections• OsteomyelitisNoteBeware of simplification. A “multiple-hit hypothesis’* is now favored for the common cortisone-induced osleonec rosiEbook Imaging of bones and joints: Part 2
s. Cortisone results in an imltalance lielween osteoblasts and osteoclasts related Io fatty degeneration and damage to the cell membrane. Steroids dam6 Osteonecroses of the Skeletal System6.1 Anatomy, Etiology, and Pathogenesis► Anatomy. Bone varies significantly in its composition, depending on age Ebook Imaging of bones and joints: Part 2 alterations in fat metabolism resulting in increased adipogcncsis. fat cell hypertrophy, and fat emboli.6.2 Bone Infarction► Pathology. A bone infarction involving fatty marrow presents as a circumscribed lesion, while an infarct involving red marrow tends to be a poorly marginated lesion within th Ebook Imaging of bones and joints: Part 2e hematopoietic marrow. Ultimately, (he necrotic area slowly becomes surrounded by a reparative margin. Bone infarcts may become smaller over time (thEbook Imaging of bones and joints: Part 2
is is common: see r- Fig. 6.5), or may even be completely absorbed.oNoteFrom a prognostic viewpoint, a bone infarction located in the metaphysis or di6 Osteonecroses of the Skeletal System6.1 Anatomy, Etiology, and Pathogenesis► Anatomy. Bone varies significantly in its composition, depending on age Ebook Imaging of bones and joints: Part 2re irrelevant for the structural integrity of the bone and are often clinically occult. Similar areas of necrosis in the epiphysis of tubular Irones, in Hal Irones such as the ilium, and in irregularly formed bones such as the sacrum resemble metaphyseal infarctions but arc referred to as osteonecro Ebook Imaging of bones and joints: Part 2sis merely bec ause ol their location.►Clinical presentation. As a general rule, infarcts are often incidental findings. In the majority of cases thesEbook Imaging of bones and joints: Part 2
e lesions arc asymptomatic; however, they may be associated with chronic or acute pain, with the latter often occurring with acute infarctions related6 Osteonecroses of the Skeletal System6.1 Anatomy, Etiology, and Pathogenesis► Anatomy. Bone varies significantly in its composition, depending on age Ebook Imaging of bones and joints: Part 2ble, with subsequent poorly marginated rarefaction of the trabeculae (► Fig. 6.1). Reparative tissue develops at the edge of the infarct and slowly mineralizes to become evident as a peripheral sclerotic margin surrounding an area of central lucency (► Fig. 6.2). Extensive, intralesionalcalcificatio Ebook Imaging of bones and joints: Part 2ns are recognizable in (he later stages. In ver}'' rare cases, metaphyseal and diaphyseal infarcts result in periosteal reaction and a widening of theEbook Imaging of bones and joints: Part 2
bone.►NUC MED. In the initial phase a “cold spot” (i.e., decreased uptake) will be present in the area of necrosis, and eventually a “cold in hot spo6 Osteonecroses of the Skeletal System6.1 Anatomy, Etiology, and Pathogenesis► Anatomy. Bone varies significantly in its composition, depending on age Ebook Imaging of bones and joints: Part 2ion within yellow, fatty marrow, will demonstrate fatequivalent signal in its center on T1W sequences. The area is typically bordered by a low-signal intensity margin, although the appearance may vary depending on the age of the infarct (* Figs. 6.3c, ► 6.4b, and ► 6.5). A hyperintense line (granula Ebook Imaging of bones and joints: Part 2tion tissue; ► Figs. 6.3b and ► 6.4a) is often present around the zones of necrosis on fat-suppressed water-sensitive sequences (see ► Fig. 6.3c). OnEbook Imaging of bones and joints: Part 2
T2W sequences without fat suppression (not routinely used) a “double-line sign” may be seen. Areas of cystic degeneration (fluid signal intensity on T6 Osteonecroses of the Skeletal System6.1 Anatomy, Etiology, and Pathogenesis► Anatomy. Bone varies significantly in its composition, depending on age Ebook Imaging of bones and joints: Part 2matopoietic marrow or with pathologic bone marrow infiltration displays an area of low signal intensity on T1W images (provided it is visible at all against the already dark marrow) and increased signal intensity on fat-saturated PDW or T2W sequences (► Fig. 6.6). The enhancement pattern of an infar Ebook Imaging of bones and joints: Part 2ct after contrast administration reflects its pathophysiology: If the diagnosis is made early, there is little or no contrast enhancement within (he cEbook Imaging of bones and joints: Part 2
enter of the infarction. Later, strong marginal enhancement of the entire border zone will be seen. With advancing age of the infarction, the nonenhan6 Osteonecroses of the Skeletal System6.1 Anatomy, Etiology, and Pathogenesis► Anatomy. Bone varies significantly in its composition, depending on age Ebook Imaging of bones and joints: Part 2f a bone infarct within yellow marrow is established by the detection of fat within the lesion on MRI. Other lesions containing fat include:•Bone lesions with the potential for spontaneous remission (fibrous cortical defect, a brown tumor in renal osteodystrophy). Ebook Imaging of bones and joints: Part 2Gọi ngay
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