BackgroundComplete cranial cruciate ligament rupture (CR) is a common cause of pelvic limb lameness in dogs. Dogs with unilateral CR often develop contralateral CR over time. Although radiographic signs of contralateral stifle joint osteoarthritis (OA) influence risk of subsequent contralateral CR, this risk has not been studied in detail.Methodology/Principal FindingsWe conducted a retrospective longitudinal cohort study of client-owned dogs with unilateral CR to determine how severity of radiographic stifle synovial effusion and osteophytosis influence risk of contralateral CR over time. Detailed survival analysis was performed for a cohort of 85 dogs after case filtering of an initial sample population of 513 dogs. This population was stratified based on radiographic severity of synovial effusion (graded on a scale of 0, 1, and 2) and severity of osteophytosis (graded on a scale of 0, 1, 2, and 3) of both index and contralateral stifle joints using a reproducible scoring method. Severity of osteophytosis in the index and contralateral stifles was significantly correlated. Rupture of the contralateral cranial cruciate ligament was significantly influenced by radiographic OA in both the index and contralateral stifles at diagnosis. Odds ratio for development of contralateral CR in dogs with severe contralateral radiographic stifle effusion was 13.4 at one year after diagnosis and 11.4 at two years. Odds ratio for development of contralateral CR in dogs with severe contralateral osteophytosis was 9.9 at one year after diagnosis. These odds ratios were associated with decreased time to contralateral CR. Breed, age, body weight, gender, and tibial plateau angle did not significantly influence time to contralateral CR.ConclusionSubsequent contralateral CR is significantly influenced by severity of radiographic stifle effusion and osteophytosis in the contralateral stifle, suggesting that synovitis and arthritic joint degeneration are significant factors in the disease mechanism underlying the arthropathy.

Photoactivation of titanium dioxide nanoparticles (TiO2NPs) can produce reactive oxygen species (ROS). Over time, this has the potential to produce cumulative cellular damage. To test this, we exposed zebrafish (Danio rerio) to two commercial TiO2NP preparations at concentrations ranging from 0.01 to 10,000 ng/mL over a 23 day period spanning embryogenesis, larval development, and juvenile metamorphosis. Fish were illuminated with a lamp that mimics solar irradiation. TiO2NP exposure produced significant mortality at 1 ng/mL. Toxicity included stunted growth, delayed metamorphosis, malformations, organ pathology, and DNA damage. TiO2NPs were found in the gills and gut and elsewhere. The two preparations differed in nominal particle diameter (12.1 ± 3.7 and 23.3 ± 9.8 nm) but produced aggregates in the 1 μm range. Both were taken up in a dose-dependent manner. Illuminated particles produced a time- and dose-dependent increase in 8-hydroxy-2'-deoxyguanosine DNA adducts consistent with cumulative ROS damage. Zebrafish take up TiO2NPs from the aqueous environment even at low ng/mL concentrations, and these particles when illuminated in the violet-near UV range produce cumulative toxicity.

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