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MRI for Assessing Erosion and Joint Space Narrowing in Inflammatory

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MRI for Assessing Erosion and Joint Space Narrowing in Inflammatory MRI AND ULTRASOUND IN DIAGNOSIS AND MANAGEMENT MRI for Assessing Erosion and Joint Space Narrowing in Inflammatory Arthropathies Mahnaz Momeni and Kathleen Brindle Rheumatology Division and Department of Radiology, The George Washington University, Washington DC, USA The superior soft tissue contrast and multiplanar capability of magnetic resonance imaging has contributed to earlier diagnosis and implementation of effective treatment for a variety of arthropathies. Owing to overlapping clinical signs and symptoms, MRI plays a role in delineating the features and stages of these conditions. With the advent of disease-modifying therapies, it is important to diagnose inflammatory arthropathy as early as possible. In this chapter, we discuss the pathophysiology of bone erosion and joint space narrowing, as well as the role of MRI in the imaging of the seropositive and seronegative inflammatory arthropathies. Key words: erosion; joint space narrowing; magnetic resonance imaging Introduction therapy early, before severe secondary disabil- ity has occurred. Assessment of the severity of On the basis of epidemiological data,1 the disease on the baseline scans of individual rheumatoid arthritis affects 1% of the popu- patients may allow clinicians to tailor their drug lation. The disease demonstrates slow progres- regimens appropriately. sion in some patients, whereas it rapidly de- stroys joint spaces and periarticular bone in others. The peak onset of symptoms is between Pathophysiology for Joint Space the fourth and the sixth decades; however, juve- Narrowing and Bone Erosion nile rheumatoid arthritis is also well known. Be- in Rheumatoid Arthritis fore the development of MRI, clinicians had to rely on clinical examination, presenting symp- The chronic inflammatory arthritides are of- toms, and radiographs to diagnose this disease. ten associated with localized and generalized Unfortunately, radiographs demonstrate only bone loss. Localized bone loss manifests as pe- the late changes owing to rheumatoid arthritis. riarticular osteopenia and subchondral bone MRI is able to detect early synovial changes erosions and constitutes an important feature in before the development of erosions. Recent re- diagnosing and directing treatment in rheuma- search also suggests that bone marrow edema toid arthritis (RA), psoriatic arthritis (PsA), and detected by MRI may, in fact, be predictive juvenile idiopathic arthritis. MRI has now re- of erosions.2 Early diagnosis is of high priority vealed that erosions occur early in these dis- in the initial workup of patients with suspected eases. Furthermore, erosions tend to correlate rheumatoid arthritis. Confirmation of the diag- with ongoing disease activity and joint destruc- nosis allows clinicians to start disease-modifying tion. Early intervention to alter the natural pro- gression of joint destruction has been shown to substantially improve functional status. The Address for correspondence: Dr. Mahnaz Momeni, Assistant Profes- revelation that erosions reflect ongoing disease sor of Medicine, George Washington University, Rheumatology Division, 2150 Pennsylvania Ave NW 3–416 Washington DC, USA 20037. voice: activity and are thus associated with an unfa- 202–741-2488. [email protected] vorableprognosisledtoincreasedtheefforts MRI and Ultrasound in Diagnosis and Management: Ann. N.Y. Acad. Sci. 1154: 41–51 (2009). doi: 10.1111/j.1749-6632.2009.04384.x C 2009 New York Academy of Sciences. 41 42 Annals of the New York Academy of Sciences to identify the underlying mechanisms behind ligand (RANKL), thereby downregulating the this pathologic process. Success of the antitu- RANKL signaling through receptor activator mor necrosis factor- (anti-TNF-) therapy in re- of nuclear factor κB (RANK). In this manner tarding and, in some cases, possibly reversing it inhibits osteoclast differentiation, suppresses early focal bone loss has been encouraging. mature osteoclast activation, and induces OCL Osteoclasts (OCLs), cells that are uniquely apoptosis. capable of bone degradation, are consistently detected at erosion sites in all animal mod- RANK els of destructive arthritis as well as hu- RANK is a transmembrane protein that be- man RA.2 Synovial inflammation generates tu- longs to the tumor necrosis factor receptor mor necrosis factor (TNF)-alpha, macrophage (TNFR) superfamily. It is expressed primar- colony-stimulating factor (M-CSF), and re- ily in the cells of the monocytes/macrophage ceptor activator of nuclear factor-κBligand lineage, including osteoclastic precursors, B (RANKL)—cytokines that fuel osteoclastoge- and T cells, dendritic cells, and fibroblasts. nesis and arthritic bone destruction. The tar- RANK is also present on the surface of ma- geted removal of OCLs by TNF blockers, ture osteoclasts. RANKL antagonism, or genetic manipulation in animal models potently blocks this bone RANKL destruction.3–6. The discovery of OPG was soon followed by the identification of its ligand, initially term- ed “osteoprotegerin ligand” (OPG-L), which Role of Osteoclasts in Bone Erosion turned out to be identical with two previously described members of the TNF superfamily. Osteoclasts are multinucleated cells derived RANKL is a 317 amino acid peptide that also from the mononuclear cell precursors of the belongs to the TNF-superfamily. It exists in two monocyte/macrophage lineage that resorbs forms, soluble and membrane bound. RANKL bone matrix. Bone destruction in RA is mainly has been detected in synovial fibroblasts, os- attributable to the abnormal activation of teoblasts, and activated T cells from peripheral OCLs. Bone is a dynamic tissue that is con- blood as well as tissue near the pannus–bone in- stantly remodeled by bone-resorbing osteo- terface. TNF-α induces RANKL and M-CSF clasts and bone-forming osteoblasts. Dysfunc- in stromal cells and also stimulates osteoclast tion or imbalance in these cells is seen in RA. precursor cells to synergize with RANKL sig- The discovery of RANK ligand highlighted the naling.8,9 It is also reported that anti-TNF drugs central role of OCLs in the pathogenesis of induce apoptosis in synovial macrophages, sug- bone destruction in RA.7 gesting a complex action mechanism. OPG The discovery of osteoprotegerin (OPG) in Bone Erosion Provides Further 1997 was a major advance in the field of bone Evidence of a Link between biology.OPG is released in soluble form by stro- Immune System Activation mal cells/osteoblasts. In addition to bone, OPG and Bone Resorption mRNA is expressed by a number of other tis- sues, including lung, heart, kidney, liver, stom- Once the function of OPG/RANK/ ach, intestine, thyroid gland, brain, and spinal RANKL in bone remodeling was recognized, it cord. OPG inhibits the differentiation and ac- was hypothesized that RANKL may be of ma- tivity of osteoclasts by acting as a decoy receptor jor pathophysiological importance in the bone for the receptor activator of nuclear factor κB and joint destruction observed in inflammatory Momeni & Brindle: MRI for Assessing Erosion 43 arthritides such as RA. Studies by Goldring pression of RANKL on synovial cells. Inter- and Gravallese45, provided initial insights into estingly, IL-413,14 and IL-10,15 both of which the role of RANKL in the pathogenesis of are classic Th2-type cytokines, also inhibit os- focal bone erosions. Other studies have pro- teoclastogenesis,16 so the positive effect of T vided compelling evidence that both activated cells on osteoclastogenesis can only be ob- T cells from the RA synovium and synovial fi- served under strictly limited conditions. Thus, broblasts produce RANKL. Indeed it is now the actual role of T cells in osteoclastogenesis assumed that activated T cells, which play a is highly complex and may depend on the type central role in the pathogenesis of RA, may con- of prevailing cytokines.17 Under some condi- tribute to the osteoclast-mediated bone resorp- tions, T cells may not drive osteoclastogene- tion via RANKL expression. Although the role sis, even if RANKL is expressed. In the pres- of RANKL in other inflammatory diseases is ence of high levels of TNF, subosteoclastogenic not yet known, Ritchlin et al.,10 using immuno- (“permissive”) amounts of RANKL may be histochemistry, revealed striking spatial regula- sufficient for TNF to drive RANKL-mediated tion of RANK, RANKL, and OPG expression osteoclastogenesis.18 in the PsA joints. The severity of bone erosion correlated with higher circulating mononuclear OCL precur- MRI-Observed Erosion sor (OcP) numbers, which revealed a novel and Joint Space Narrowing mechanism for osteoclastogenesis in PsA.10 in Inflammatory Arthritis Magnetic resonance imaging is a sensitive The Role of T Cells modality for the detection of erosions, and it in Osteoclastogenesis does so more often and at an earlier stage than radiography.19 As RANKL is expressed in activated T cells, Fast spin-echo T1-weighted sequences, fat- it is of vital importance to determine whether saturated T2 fast spin-echo sequences, and T cells have the capacity to induce osteoclast postcontrast T1-weighted sequences with fat differentiation. Indeed, Kong et al.11 showed saturation are performed in axial, coronal, that RANKL expressed on activated T cells and sagittal orthogonal planes. If fat-saturated directly induces osteoclastogenesis. T2-weighted sequences are not available, a Helper T (Th) cells are divided into two short-tau inversion recovery (STIR) sequence main subsets according to the cytokines they can be obtained. Good fat saturation and con- produce, Th1 and Th2.12 Th1
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