Introduction: Avascular necrosis of the lunate in Systemic Lupus Erythematous (SLE) and rheumatoid arthritis (RA) are not rare. Our study aimed to describe the histopathology of the lunates after removing them in the operating room in patients with rheumatoid diseases and lunate palmar dislocation. We correlated the histopathological findings with magnetic resonance imaging (MRI), radiological parameters, and blood test parameters. Methods: From January 2006 to January 2015, 12 patients were operated for rheumatoid disorders, 8 RA, 1 SLE, and 3 psoriatic arthritis (PA). There were 8 female and 4 male with a mean age 65 (53-79) years. Antinuclear antibodies and other relevant tests were performed. Anticardiolipin antibody, anti-double-stranded DNA, and anti-β-2 glycoprotein I were measured by enzyme-linked immunosorbent assay (ELISA). All patients underwent MRI study. T1-weighted images were evaluated for bone necrosis of the lunate. In the operating room, we excised whole lunates and we studied the macroscopical aspect inside and outside. We evaluated the size, cartilage surfaces, number of foraminas, and ligament insertions. After that, we cut the bone and showed the bleeding bone and collapse areas. Histopathological analysis was performed with lunate sections. The lunates were fixed in formalin, decalcified, embedded in paraffin, and cut in 5 microm sections, and stained with hematoxylin and eosin. We visualized lunates sections by microscope. The surgical treatment was a wrist arthrodesis in 8 cases and wrist arthroplasty in the other 4 cases. We evaluated x-rays data such as lunate morphology, Stahl Index, Carpal Height ratio (CHR), and Carpal Ulnar distance ratio (CUDR). We correlated preoperative x-rays and MRI data with histopathological findings. We correlated blood test parameters with the histology. Statistical analysis of data was performed with chi-square test (significance level P < .05). Results: In 2 cases, we showed a lunate flattening associated with a partial hypointensity in coronal sections in T1-weighted images in MRI. Microscopic analysis showed synovial hyperplasia, fatty marrow, and fibrovascular tissue. We did not find avascular necrosis in any complete lunate but we found a focal necrosis (empty lacunae) in 2 cases. Mean CHR was 0.385, CUDR 0.301, Index Stahl 56.95, and radio-scaphoid angle 76°. We showed more ulnar translation in RA than in other rheumatoid disorders (CUDR P = .002). The correlation focal lunate necrosis with MRI was P = .371. The correlation focal lunate necrosis with scapholunate ligament rupture was P = .640. We showed 2 blood test parameters statistically significant with focal lunate necrosis (C reactive Protein P = .046 and Rheumatoid Factor P = .053). Conclusion: Neoangiogenesis and wrist synovitis in rheumatoid disorders, with an increased number of synovial cells and vessels, seem to contribute to the progression of autoimmune diseases. It is possible that the patients with rheumatoid wrists have hypervascularity and therefore a chronic adaptation to a decrease number of vessels in the lunate and to ligament injuries. This could avoid to have Kienböck disease in a chronic palmar lunate dislocation in rheumatoid disorders.
