Summary
Reasons for performing study: Structural changes in articular cartilage associated with the ageing process require definition for investigators performing developmental and age‐related studies, for which information is lacking.
Objectives: To 1) determine the onset and end of puberty as defined by serum insulin like growth factor (IGF‐I) and IGF‐binding protein‐3 (IGFBP‐3) concentrations and 2) correlate articular‐epiphyseal cartilage complex structural changes with the onset and end of puberty.
Methods: IGF‐1 and IGFBP‐3 were measured in serum samples from normal female and male horses age 9‐715 days to determine peak and steady‐state values for horses transitioning through puberty. Osteochondral tissue sections were obtained from horses age 120‐840 days (4‐28 months) and examined histologically for cartilage canals and tidemark formation.
Results: In male and female horses, serum IGF‐1/IGFBP‐3 concentrations peaked at approximately 225 days, defining the onset of puberty. Cartilage canals were absent from articular cartilage just prior to this time point. IGF‐1/IGFBP‐3 concentrations declined to steady‐state levels at approximately age 450 days, signalling exit from puberty and therefore the beginning of ageing. This time point correlated to initial formation of a tidemark in the osteochondral tissue sections.
Conclusions: Horses may be considered pubescent at age 225‐450 days, and post pubescent and ageing after age 450 days.
Potential relevance: Defining the normal post natal to post pubescent concentrations for serum IGF‐I and serum IGFBP‐3 establishes subsets of animals for age‐related studies and may be used to monitor horses for abnormally high IGF‐1 concentrations due to natural disease or subsequent to systemic growth hormone administration.
or the development of specific clinical outcomes. However, they have not been examined simultaneously in the same cohort of SSc patients to compare their respective predictive abilities. We compared three methods of subsetting based on: (i) extent of skin involvement; (ii) presence of SSc-specific antibodies, namely anti-centromere (ACA), anti-topoisomerase I (ATA), and anti-RNA polymerase III (RNAP) antibodies; and (iii) unsupervised clustering of the subjects. Since the clinical value of prediction is predominantly in early disease, we compared subjects with either <2 years or 2-4 years of disease duration. The five outcomes of interest were all-cause mortality, impaired health-related quality of life (HRQoL) defined by an SF-36 physical component summary score (PCS) of <40, interstitial lung disease (ILD), significant ILD defined by a forced vital capacity (FVC) of <70% predicted and pulmonary hypertension (PH). We hypothesized that the predictive abilities of different SSc subsets would depend on the outcomes being predicted and on disease duration and that it would be unlikely that one method would demonstrate superior predictive ability over any other method for all outcomes and disease durations.
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