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The purpose of this study is to use the CD15 focus score (FS) to determine the sensitivity and specificity of bacterial infection persistence in spacer-based two-stage revision arthroplasty. The analysis comprises 112 cases that were subjected to revision due to the presence of infection upon replacement of a joint endoprosthesis. The histopathological data were collected in accordance with the synovial-like interface membrane (SLIM) classification and the CD15-FS and correlated with the microbiological data (MD). The quantifying evaluation of the CD15-FS was performed without knowledge regarding the microbiological data (MD). Correlation with the MD was performed after a 14-day cultivation period. With a single evaluation (1 focus, field area: 1.2 mm2) with a score value of 42, the CD15-FS showed a sensitivity for the eradication of infections of 0.64 and a specificity of 0.79 (PPV = 0.5; NPV = 0.87). With tenfold evaluation (10 foci, field area: 12 mm2) with a score value of 220, the sensitivity for the eradication was 0.68, the specificity 0.91 (PPV = 0.7; NPV = 0.89). No statistically significant correlation between the score values and the different infectious species could be detected. Based on the MD in 112 cases the rate of infection eradication was 75%. Polymethylmethacrylate-particles (PMMA) were detected in the perispacertissue in 64 cases (58%). No significant correlation could be established between microbiological pathogen detection and the presence of PMMA. In all cases (n = 112), periimplant synovial tissue (SLIM) with variable fibroblastic cellularity, capillary proliferation, leukocytic infiltration, fibrin deposition, new formation of woven bone and detection of PMMA particles was observed. These cases were classified as type IX perispacer synovialis/SLIM: type IX‑A with histopathological infection eradication and type IX‑B with histopathological infection persistence.

This review article elucidates the differential diagnostics of malignant and benign joint tumors, pseudotumors of the joints and the peri-implant tissue, which are rare but important entities in rheumatology and orthopedic rheumatology. The tissue of origin includes the synovium, peri-implant tissue, peri-articular fibrous tissue and peri-articular osseous tissue. Pseudotumors can be viewed as independent but heterogeneous entities. These are essentially manifested as tumor-like depositions of crystals, calcareous deposits, vascular malformations, ectasia of the synovia and joint capsule tissue and pseudocysts. Other causes for pseudotumors are focal destructive inflammation (e.g. induced by foreign bodies), high grade synovitis and focal fibrinoid necrosis (i.e. rheumatoid nodules). Methodologically, these diagnostics are based on conventional standard staining methods, immunohistochemical analyses of formalin-fixed and paraffin-embedded materials and on molecular diagnostic procedures. The latter are of great importance in cases of benign and malignant joint tumors. The most important immunohistochemical markers with respect to joint tumors are S100, SM-actin, CD68, CD34, STAT6, clusterin, Muc‑4, beta-catenin and MDM2-FISH. The following markers are recommended for the differential diagnostics and typing of periarticular tumor metastases in the pathology of rheumatic diseases: AE1/AE3, CK8, p63, TTF‑1, TGB, PSA, androgen receptor, GATA, CD56, chromogranin, CDX‑2, SAT-B2, SALL4, estrogen and progesterone receptors, CD45LCA, CD30, CD79a and S100. Necrosis, inflammatory infiltrations and reparative inflammatory changes may complicate the histopathological classification. Therefore, a correlation with clinical, microbiological and radiological data in the sense of interdisciplinary synergistic diagnostics may be required.

Bei der aseptischen Knochennekrose handelt es sich um einen Gewebstod und somit um eine Nekrose des Lamellenknochengewebes. Die Bezeichnung aseptisch bezieht sich auf die kausale Pathogenese: Es handelt sich daher nicht um eine infektios, septisch induzierte Knochennekrose wie bei der infektiosen akuten Osteomyelitis. Formalpathogenetisch konnen zwei divergente Pathogeneseprinzipien vorliegen: (1) eine Minderdurchblutung des Lammellenknochens im Sinne einer ischamischen Nekrose oder (2) eine direkte toxische Schadigung von Osteozyten und Osteoblasten mit der Folge von Apoptosen oder Knochennekrose. Die Ursachen der Minderdurchblutung sind vielfaltig und umfassen: vaskulare Malformationen, Koagulopathien, Hamoglobinopathien, maligne hamatologische Erkrankungen, Luftembolien, Dekompressionserkrankungen, Makro- und Mikrotraumata und Vaskulitiden. Die Ursachen fur die direkte Osteozyten‑, Osteoblasten-toxische Schadigung beinhalten im Wesentlichen den Alkoholabusus, medikamentose Therapien (z. B. Chemotherapeutika, Kortison) und Storungen des Lipidmetabolismus. In aktuellen molekularen und zellularen Pathogenesemodellen wird von einer „Dysbalance“ der katabolen und anabolen ossaren Stoffwechselprozessen in Osteozyten und Osteoblasten ausgegangen. Fur die molekulare Pathogenese spielen das RANKL-RANK-System, das ROS-System und die PPAR-Gamma-Signaltransduktion eine wesentliche Rolle. Die histopathologische Differenzialdiagnose einer aseptischen Huftkopfnekrose ist umfassend, beinhaltet alle fokalen ossaren Veranderungen, in welchen Knochennekrosen im unterschiedlichen Ausmas auftreten konnen: infektiose Osteomyelitis, chronische immunologisch bedingte Osteomyelitiden, Pseudarthrose, infizierte Pseudarthrose, Frakturen, Luxation, Epiphysenschaden sowie maligne metastatische intraossare Erkrankungen und nichtmetastatische intraossare malignen Erkrankungen.