Our case of SS presented with LBP, and upon examination, multiple lesions were identified in the axial skeleton, including the LFJs, bilateral SI joints, and vertebral arch. To our surprise, an inflammatory lesion was also found in the symphysis pubis. To our knowledge, this is the first case having such findings.

Systemic manifestations of SS encompass various systemic organs and tissues, including the musculoskeletal system [20]. SS often leads to systemic manifestations that primarily involve the musculoskeletal system, specifically tissues of bone, joint, synovium, and cartilages, with sparing the musculacture [21]. Additionally, the significant prevalence of thyroid disease in those SS implicates potential disruptions in bone and cartilage metabolism, calling for more detailed analysis. In patients with SS, 96% experience peripheral joint pain, while 1.8% develops arthritis. Reports indicate that arthritis rates can be as high as 70% [22,23]. In our case, the patient also presented with peripheral joint pain, including morning stiffness in both hands and chronic pain in the PIPs for years. Additionally, our patient exhibited axial skeleton involvement, a condition that is relatively rare among those with SS. Although sacroiliitis and facet joint syndrome could potentially be attributed to age-related degeneration [5,8-10,24], several factors raised the possibility that SS may play a significant role in the coexistence of these conditions like our case. We will explore these factors in detail in the following discussion.

With respect to the facet joint syndrome, the LFJ is unique as the only pure synovial joint within the spine, undergoing a degenerative course akin to that observed in appendicular joints, which course encompasses the changes in joint capsule, subchondral bone, cartilage, synovium, and adjacent soft tissues [24]. Therefore, it is plausible that SS may also lead to the development of LFJ syndrome, as synovitis in appendicular joints is a common symptom of SS. Moreover, the primary etiology of the facetogenic pain is degenerative osteoarthritic changes of the facet joint, which condition is intimately linked to the degeneration of the spinal discs, a process often correlated with significant physical labor performed before the age of 20 [24]. Our patient is a housewife with no history of heavy labor or intervertebral disc degeneration, we have excluded these mentioned common causes, leading us to consider that SS may play a key role in the development of her skeletal disorders.

Next, we address the characteristics of sacroiliitis. The coexistence of Inflammatory Back Pain (IBP) and SS was first described in 2006 by Chang et al. [26], who identified this coexistence as an unusual discovery. Eren et al. [27] found lately that patients with primary SS had a elevated prevalence of IBP (24.7% vs. 4%) and sacroiliitis (10.5% vs. 2%) compared to controls. Ankylosing spondylitis is the primary disorder associated with IBP and sacroiliitis [28,29]. However, our case developed sacroiliitis in the absence of ankylosing spondylitis and with negative HLA-B27 status, suggesting that SS may contribute to the development of sacroiliitis.

This case is notable for identifying a symphysis pubis lesion via SPECT/CT imaging. While the etiology of osteitis pubis (pubalgia) is unclear, it is commonly linked to repetitive trauma and shear forces across the symphysis pubis in athletes [30-34], often due to opposing forces from the rectus abdominis muscles and the adductor longus during activities like kicking or rapid directional changes [35]. It is widely accepted that lesions in the symphysis pubis are closely related to the muscles attached to this anatomical site. Traditionally, osteitis pubis is observed more frequently in men than in women, with previous studies indicating a prevalence 2 to 5 times higher in men [36]. Notably, our patient is a non-athletic female housewife, making it challenging to attribute her symphysis pubis lesion to the athletic-related causes. This necessitates consideration of other, less common pathological conditions. In this context, it is plausible that the lesion may be associated with SS, suggesting a potential impact of SS on the axial skeleton that has not been extensively recognized.

However, there are some contradictions to consider. Firstly, facet joint syndrome is characterized by cartilage erosion and inflammation [3], whereas SS typically leads to non-erosive synovitis [37]. Although rare, there are instances of SS presenting with erosive arthritis, so it cannot be entirely ruled out that SS may lead to facet joint syndrome [38]. Secondly, patients with SS may develop autoimmune thyroiditis, which can result in hypothyroidism [39]. In our case, she had autoimmune thyroiditis. Thyroid hormones have been known to affect the cell proliferation and tissue differentiation of bone/cartilage cells, and the hypothyroid state appears to induce decreased bone resorption and turnover [40], which contradicts the pathological phenomena observed in facet joint syndrome. Facet joint syndrome is typified by increased subchondral bone resorption and turnover [24]. Based on the above, it is evident that the thyroiditis associated with SS is unrelated to facet joint syndrome, and SS does not affect the facet joints through this pathophysiology.