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病例漫谈109:膝关节骨性关节炎患者诱发膝关节疼痛的可能病因—骨质改变 [复制链接]

Osteoarthritis (OA) is characterized by degeneration and destruction of articular cartilage that results in pathological bone changes. In recent studies on the relationship between OA progression and bone lesions, alterations were found to occur ahead of obvious cartilage degeneration and OA. Joint pain also frequently indicates the presence of microfractures, as do signal alterations in bones in magnetic resonance imaging (MRI) of patients with hip joint pain. Although we have reported that the pathophysiology of hip OA presumably includes bone alteration, the pathogenesis of bone changes in this context is still largely unknown.

There exist numerous studies on the relationship between OA and MRI findings. In this report, we describe a patient with knee OA and the associations among the pathophysiologies of OA, joint pain, and MRI findings.

Case Report
An 86-year-old man presented at our institution with severe right knee joint pain in May 2011. The patient complained of right lower leg edema that had coincided with the occurrence of joint pain. The edema persisted until the knee pain stopped. Alendronate administration was begun in October 2011 immediately after he was diagnosed as having osteoporosis. His knee pain had become greatly improved by May 2012. At the first visit, plain radiographs revealed a bone cyst and joint space narrowing (Figure 1A, 1B) (Kellgren and Lawrence grading [KL] grading Ⅱ). Two years later, his joint pain had disappeared. At that time, plain radiographs showed increased joint space narrowing (KL grading Ⅱ) and localized bone formation (Figure 2A, black arrow) at the proximal lateral side of the tibia and MRI analysis depicted a cyst in the proximal medial tibia (Figure 2B, 2C). Three months later, his knee pain returned. MRI examination disclosed broad signal changes in the distal medial femur and in the proximal medial tibia by T1-weighted imaging (T1W) (TR: 530 [SI], FA: 90 [SI], and TE: 14 [SI]) and short t inversion recovery (STIR) (TR: 5010 [SI], FA: 180 [SI], TE: 71 [SI], and TI: 150 [SI]) (Figure 3A, 3B). Plain radiographs showed no OA progression or localized bone formation at the proximal lateral side of the tibia (data not shown). Four months afterwards, his knee joint pain was improved, but plain radiographs revealed further joint space narrowing and localized bone formation (Figure 4B, black arrow) at the proximal lateral side of the tibia (KL grading Ⅱ) (Figure 4A, 4B).
2011年5月,一名86岁男性到我们机构就诊,患者右膝关节疼痛严重,主诉右小腿水肿,水肿持续直到膝盖疼痛停止。2011年10月,患者被确诊为骨质疏松症,随即接受了阿仑膦酸盐治疗。到2012年5月,患者膝盖疼痛已得到很大改善。首次就诊时,X线平片显示骨囊肿和关节间隙狭窄(图1A,1B)(Kellgren-Lawrence[KL]分级,评分为Ⅱ级)。两年后,关节不再疼痛。当时,X线平片显示胫骨近端外侧关节间隙变窄(KL评分为Ⅱ级),存在局部骨形成(图2A,黑色箭头),MRI分析结果显示胫骨近端内侧出现囊肿(图2B,2C)。三个月后,患者再次出现膝盖疼痛。通过T1加权成像(T1W)(TR:530 [SI],FA:90 [SI]和TE:14 [SI])和短时间反转恢复序列(STIR)(TR:5010 [SI],FA:180 [SI],TE:71[SI]和TI:150 [SI])(图3A,3B)的MRI检查,发现远端股骨内侧和胫骨近端内侧信号变宽。X线平片显示胫骨近端外侧没有出现骨性关节炎发展或局部骨形成(数据未呈现)。四个月后,患者膝关节疼痛得以改善,但X线平片显示胫骨近端外侧关节间隙变窄,出现局部骨形成(图2A,黑色箭头)(KL评分为Ⅱ级)(图4A,4B)。

Figure 1. Plain radiograph displaying a bone cyst and joint space narrowing, but no localized bone formation at the proximal lateral side of the tibia (KL grading Ⅱ). (A) frontal view, (B) lateral view.

图1. X线平片显示胫骨近端外侧出现骨囊肿和关节间隙变窄,但局部无新骨形成(KL评分为Ⅱ级)。  (A)前视图,(B)侧视图。

Figure 2. Plain radiographs revealing progressed OA and localized bone formation (A; black arrow) at the proximal lateral side of the tibia (KL grading Ⅱ) (A; frontal view). Osteonecrosis in the  proximal medial tibia was seen by T1W (B; white arrow) and STIR (C; white arrow).

图2. X线平片显示胫骨近端外侧出现骨性关节炎发展和局部骨形成(图A,黑色箭头)(KL评分为Ⅱ级)(A;前视图)。T1W(B;白色箭头)和STIR(C;白色箭头)显示胫骨近端内侧存在骨坏死。

Figure 3. MRI indicating broad signal changes in the distal medial femur and in the proximal medial tibia by T1W (A) and STIR (B).

图3. T1W(A)和STIR(B)磁共振成像显示股骨远端内侧以及胫骨近端内侧信号变宽。    

Figure 4. Plain radiograph demonstrating progressed joint space narrowing and localized bone formation (B; black arrow) at the proximal lateral side of the tibia (KL grading Ⅱ). (A) frontal view, (B) lateral view.

图4. X线平片显示胫骨近端外侧出现进行性关节间隙变窄和局部骨形成(图 A,黑色箭头)(KL评分为Ⅱ级)。(A)前视图,(B)侧视图。

The patient was informed that data from the case was desired for publication and he gave his consent.

We encountered an aged man with knee OA. Plain radiographs at his first visit showed mild OA-like features. MRI analysis revealed a medial tibial cyst during the pain-free period and broad bone signal changes in the joint at the time of severe knee pain. The OA later progressed radiographically to a more severe stage, suggesting that the cause of OA and joint pain may have been bone alterations in the knee, as also seen in a hip joint we described previously.

Muraki et al. have reported that in a sample of Japanese individuals over 60 years of age, 47.0% of men and 70.2% of women had radiographic knee OA. However, the incidence of knee pain among the patients was only 21.2% and 27.3% respectively. Clegg et al. have observed that joint pain had spontaneously improved 6 months after onset in a non-medicated group. These results suggest that many OA patients do not have joint pain. Furthermore, it seems that knee joint pain in most OA patients improves naturally.

There exist numerous reports on the relationship between knee OA and bone marrow lesions (BMLs) in knee MRI proposing that BMLs change over time and contribute to the pathophysiology and progression of radiographic knee OA. In one of the largest studies of its kind, Sofat et al. reported that knee joint pain was found in 77.5% of individuals with knee OA and BMLs. In our patient, broad bone alterations detected by MRI were observed in the medial knee joint. These findings strongly suggest that the pathophysiology of knee OA and joint pain are BMLs. Our data also showed no apparent relationship between radiographic OA features and joint pain, but rather that OA progressed after bone signal changes were detected by MRI. This evidence implies that the bone is the primary region of OA occurrence and progression.

Taljanovic et al. have compared MRI findings with histology in 19 hip OA subjects who had undergone hip surgery. The authors concluded that bone marrow edema detected by MRI in hip OA correlated with the severity of pain, radiographic findings, and microfractures. Other groups have recently described that such MRI signal changes in joints frequently suggest microfractures. We also have reported that bone changes could be the primary cause of hip OA and that the pathophysiology of hip OA could be microfractures. Collectively, this body of evidence strongly implicates microfractures with knee OA pathophysiology.
Taljanovic等人比较了19例髋关节骨关节炎患者的MRI结果和组织学信息,上述患者均进行过髋关节手术。他们认为从髋关节骨性关节炎患者MRI结果可看出骨髓水肿与严重疼痛、影像学表现和细微骨折三者之间存在联系。近期,另一些研究人员报道,认为关节MRI检测的信号改变表明了细微骨折的存在。我们同样报道了骨质改变可能是引起髋关节骨性关节炎的主要原因,髋关节骨性关节炎的病理生理学病因可能是细微骨折。 总的来说,这一证据已经证实了细微骨折与膝关节骨性关节炎的病理生理学有关。

Lastly, we detected localized bone formation at the proximal lateral tibia in a follow-up plain radiograph that had not been radiographically evident at the first visit, indicating that bone formation had apparently increased over time. This finding resembled the callus observed in the process of general fracture healing. It is currently not known why or how localized bone formation is present in OA. However, because imaging reflected OA progression in this case, localized bone formation might also be a hallmark of bone microfractures and knee OA progression.

We encountered the case of an aged man with knee OA whose plain radiograph and MRI findings revealed OA progression that was potentially due to bone alterations. Specifically, microfractures may be implicated with OA pathogenesis.

由MediCool医库软件 王露黔 编译

原文来自 Am J Case Rep

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