Synovasure has been designed and validated for use in the diagnosis of periprosthetic joint infection (PJI). It has a reported sensitivity of 97.4% (CI 86.1–99.6%) and specificity of 95.8% (CI 90.5–98.6%), higher than the variable results reported for aspiration by most units. At a cost of £500 per test, we aimed to establish cost-effectiveness and diagnostic accuracy, to determine its role in routine practice. We developed a protocol for pre-operative aspiration or intra-operative use. Prerequisites for entry were a high index of clinical suspicion for PJI and equivocal standard investigations. All cases were discussed at the lower limb arthroplasty MDT and approved only if use would change clinical management. Over 15 months, 36 tests were approved for 22 aspirations (5 hip, 17 knee) and 14 intra-operative cases (7 hip, 7 knee). 10/36 had undergone previous revision surgery. 35/36 cases complied with the protocol. All 22 Synovasure aspirations were negative, corresponding to the microbiology in all but one case; thought to be a contaminant. In the intra-operative group there was one true positive and 12 true negative tests, giving a sensitivity of 100% (95% CI 2.5–100%) and a specificity of 100% (95% CI 73.5–100%). Synovasure influenced decision making in 34/36 procedures. One test failed and in another there was evidence of frank infection. In 11 cases no surgery was performed versus a potential two-stage revision and in 21 cases a single rather than two-stage revision was performed. Resulting in estimated savings of £686,690, offset against a cost of £18,000. The Synovasure test was found to be sensitive and specific and can aid decision-making particularly in complex cases with an equivocal diagnosis of PJI. The use of this test through a robust protocol driven peer review MDT process not only reduces patient morbidity but drives significant efficiency savings.
Outcome measures used were post operative mortality, Post operative improvement in Frankel score, level of pain perception, level of mobility and ability to perform activities of daily living.
Mean (95%CI) pre-op Physical Component Summary score (PCS) was 28.1 (26.6–29.5). This increased at last F/U to 39.3 (36.9–41.7, P<
0.0001). Mean Mental Component Summary score (MCS) was 47.8 (45.5–50.1) pre-op and 52.3 (50.2–54.5) at last F/U (P=<
0.0001). While there was no difference in patient demographics, a significant difference existed in the pre-op SF-12 scores between the patients of the two surgeons (mean PCS: 24.9 (22.7–27.0) vs. 29.6 (27.8–31.5) and MCS: 44.0 (39.3–48.6) vs. 49.5 (46.8–52.1)). No significant difference was found in the improvements in mean SF-12 scores between these two patient groups (PCS: 12.3 (7.6–17.1) vs. 10.8 (8.3–13.3) and MCS: 6.3 (1.8–10.8) vs. 3.0 (0.3–5.6)) or in the SF-12 scores at 12-months (PCS: 37.2 (32.8–41.6) vs. 40.2 (37.2–43.2) and MCS: 52 (48.3–55.7) vs. 52.3 (50.1–54.4)). No significant difference was found between post-op PCS of the less disabled patient group or MCS scores of either group and published SF-12 age-matched population norms (65–74 years: mean PCS of 44.4 (42.7–46.1) and MCS of 53.8 (52.7–55.0)). Three published series (869 patients) were located providing SF-12 data for TKR surgery. Weighted mean age was 69 years and pre-op PCS was 30 (range:27–34). 12-month improvement in PCS was 7.0 (range:7–8.5). For THR, one paper (147 patients from 3 hospitals) containing SF-12 data was found. Mean age was 68 years (range:36–89). Mean pre-op PCS and MCS of 30.5 and 41.4, increased to 45.6 and 49.7 at one year.
The adjusted odds ratios for pelvic osteophytes and HO with carriage of the rare FRZB 200 variant were 4.34 (1.01–18.7 p=0.048) and 1.64 (1.05 to 2.54, p=0.028) respectively. The adjusted odds ratio for osteolysis was 0.62 (0.38 to 0.99 p=0.049). There were no bone phenotype associations with the FRZB Arg324Gly variants.
Fracture repair is a complex physiological process during which bone shows the remarkable ability to mount a repair process, restoring its mechanical integrity and anatomical configuration by original osseous tissue. Programmed cell death, or apoptosis, is a naturally occurring cell suicide pathway with a homeostatic function in the maintenance of continuously renewing tissues. The present study investigated the relation between cell proliferation and cell death (apoptosis) during fracture healing in a mouse femoral model. Left femoral osteotomies were performed in 20 male CFLP mice (35–45g), immobilised with uniplanar external fixators. 4 animals were sacrificed on days 2, 4, 8, 16 and 24 post-fracture and fracture callus collected for paraffin embedding. Localisation of cell proliferation was examined using immunohistochemistry with proliferating cell nuclear antigen (PCNA) monoclonal antibody. Apoptotic cells were visualised with the terminal deoxynucleotidyl transferase (TdT)–mediated dUTP-biotin nick end-labelling (TUNEL) method. Random images of each time specific specimen were captured via a digital camera and the positive labelling indices of PCNA and TUNEL labelling were calculated and statically compared. Cell proliferation and apoptosis were found co-existing during the entire period of fracture healing studied. Cell proliferation was predominant in the early phases of fracture healing (days 2–8). PCNA positive labelling index peaked at day 8 (p<
0.01, t-test) and PCNA-positive cells were not limited to the fracture gap mesenchymal tissues but extended in the periosteum along most of the fractured femur. TUNEL positive labelling was minimal in the early stages (days 2–8). In later stages of fracture healing (days 16–24), PCNA expression declined as intramembranous and endochondral ossification spread within the fracture site and apoptosis was the dominant cell activity with the TUNEL positive labelling index peaked at day 16 (p<
0.05, t-test) and then declined sharply at day 24. The current study indicated that apoptosis was a normal concomitant during fracture repair, confirming programmed cell death in chondrocytes and bone cells, and that cell proliferation and apoptosis were tempero-spatially dependent. These findings support the view that apoptosis is a natural process, genetically programmed and active during fracture repair. The demonstration of a mixture of proliferative and apoptotic cell populations in the regenerating tissues of fracture callus, suggests that apoptosis and cell proliferation may be regulated by local factors during fracture healing.