Laboratoire Central d'Anatomie Pathologique, Hôpital L. Pasteur, University of Nice, Nice, France.
Nail's Dermatology Consultations, Cannes, France.
Am J Dermatopathol. 2021 Dec 1;43(12):898-902. doi: 10.1097/DAD.0000000000001947.
The aim of this analysis was to re-examine the classical concept of distal interphalangeal joint (DIP) psoriatic arthritis (PsA) as an entheseal-driven disease. Two cadaveric fingers with severe psoriatic arthritis were analyzed. Our results demonstrate that inflammation of DIP PsA is multifocal without interconnection between entheses and articular cartilage of the DIP. We found a clear association between synovitis and focal loss of articular cartilage at the head of the intermediate phalanx. By contrast, the articular cartilage adjacent to the zone of severe enthesitis did not show notable damage. Fibrocartilaginous destructions of enthesis were characterized by either a multifocal lymphocytic inflammation, accompanied by osteoclastic resorption, beginning on the interface between the uncalcified and calcified fibrocartilage and then extending into the bone or a subchondral bone inflammation which insidiously destroyed first the bone and then the fibrocartilage. Some sections well showed an inflammation either mild or prominent starting at the level of vascular foramina of flexor enthesis, with secondary invading into the interface between bone and enthesis. The different anatomic sites examined showed a slight predominance of CD8+ T cells over CD4+ T cells: 52% up to 63% for CD8+ T cells vs. to 36% up to 48% for CD4+ T cells. Sparse interspersed CD1a+cells and PS100+cells were also seen with a predominance of PS100+ cells on CD1a+ cells. CD20+ B cells, plasmocytes, neutrophils, and mastocytes were absent or rare. CD123 positive cells were not observed. In DIP PsA, 3 findings predominate: (1) cartilage invasion by the thin pannus offers a more rational explanation for the focal joint destruction than does inflammation of the enthesis which is independent from articular cartilage, (2) the thick ventral plate and to a lesser extend the thin dorsal plate constitute a barrier between the inflamed entheses and the articular cartilage, and (3) an unusual form of minute vascular foramen contributes to the early stage of enthesitis. This small study suggests that DIP PsA is a complex disease. It affects anatomical micro sites which, although close, are in fact relatively independent of each other. Further studies are needed to test this hypothesis.
这项分析的目的是重新检验经典的远端指间关节（DIP）银屑病关节炎（PsA）作为附着点驱动疾病的概念。对 2 个严重银屑病关节炎的尸体手指进行了分析。我们的结果表明，DIP PsA 的炎症是多灶性的，没有附着点和 DIP 关节软骨之间的连接。我们发现滑膜炎与中间指骨头部关节软骨的局灶性丧失之间存在明确的关联。相比之下，与严重附着点炎相邻的关节软骨没有明显的损伤。附着点的纤维软骨破坏的特征是在未钙化和钙化纤维软骨的界面上出现多灶性淋巴细胞炎症，伴有破骨细胞吸收，然后向骨内扩展，或者是在软骨下骨炎症，它首先侵蚀骨，然后侵蚀纤维软骨。一些切片显示，炎症要么轻微，要么突出，起始于屈肌附着点的血管孔水平，然后继发性地侵犯骨与附着点的界面。检查的不同解剖部位显示 CD8+T 细胞略多于 CD4+T 细胞：52%至 63%为 CD8+T 细胞，36%至 48%为 CD4+T 细胞。也可见稀疏散在的 CD1a+细胞和 PS100+细胞，CD1a+细胞上以 PS100+细胞为主。未见 CD20+B 细胞、浆细胞、中性粒细胞和肥大细胞。CD123 阳性细胞未观察到。在 DIP PsA 中，有 3 个发现占主导地位：（1）薄的滑膜侵入软骨为局灶性关节破坏提供了比附着点炎症更合理的解释，而附着点炎症与关节软骨无关；（2）厚的腹侧板和较小程度的薄背侧板构成了炎症附着点和关节软骨之间的屏障；（3）一种不寻常的微小血管孔形式有助于附着点炎的早期阶段。这项小型研究表明，DIP PsA 是一种复杂的疾病。它影响解剖学上的微小部位，尽管这些部位接近，但实际上彼此相对独立。需要进一步的研究来验证这一假设。
