Long bone growth during prolonged intermittent corticosteroid treatment and subsequent rehabilitation

Abstract

Immature A/J mice were treated for up to 7 weeks intermittent doses of triamcinolone hexacetonide and were thereafter allowed to recover for 7 weeks. Qualitative and quantitative morphological measurements were performed on the epiphyseal cartilage plate and diaphyseal bone of the humerus. By the third injection significant structural changes were noted in the cartilaginous tissue followed by a complete cessation of bone growth. The hormonal inhibitory effect on long bone growth lasted throughout the experimental period. However, at the end of the recovery period the length of the humerus was 96% of the normal. In contrast, the humeral width at midshaft and the width of its medullary cavity revealed slower recovery, achieving only 80% of the control values. Following rehabilitation, the growth of experimental epiphyseal plates exceeded that of nontreated animals as their width and the number of hypertrophic chondrocytes were 131% and 125% of their controls respectively. Thus, in A/J mice (a highly susceptible inbred strain of mice) intermittent (every four days) administration of a long-acting corticosteroid hormone arrested endochondral and periosteal bone formation; the former, however, underwent full recovery following the termination of the hormonal treatment.

Bone deficit in ovariectomized rats. Functional contribution of the marrow stromal cell population and the effect of oral dihydrotachysterol treatment.

“…Other mechanisms such as immunologically based cellular interactions or "systemic changes" in endocrine sensitivity of bone cells (e.g., parathyroid hormone) could also be involved, but ifpresent, these are probably oflesser importance (23). Here, cells removed from the constraint of a hypothetically unfavorable local intraosseous microenvironment rapidly recovered and proved superior to cells biopsied from normal rats in their ability to proliferate and mature (viz Millipore Diffusion Chambers); the outcome resembled a catch-up growth phenomenon (24)(25)(26). Vitamin D metabolites and analogues may operate at these different levels in bone.…”

Infant lower extremity long bone growth rates: comparison of contemporary with early 20th century data using mixed effect models

“…While the long bones lengthen mainly by enchondral ossification at the physes, there is a modest contribution to longitudinal growth from enchondral ossification at the spherical growth plate of the epiphysis. Infancy marks the period of maximal bone growth and thus it is also the period most susceptible to growth alterations due to environmental stressors such as nutrition, diseases, chemical exposures, and mechanical stimuli (Carter, Van Der Meulen, & Beaupre, ; Eckhardt, Suchindran, Gordon‐Larsen, & Adair, ; Prentice et al, ; Savendahl, ; Silbermann, Levitan, Kleinhaus, & Finkelbrand, ; Turner, ; Whitfield, Morley, & Willick, ; Wu, Legido, & De Luca, ). These factors further complicate the analytical modeling of infant bone growth.…”

Binding sites in fetal and growth plate cartilage

“…The second major physiologic process that is hormone dependent is, of course, the rate of linear growth. In earlier in vivo animal experiments using hormone excesses or deficiencies, growth hormone, insulin, thyroid hormone, corticosteroids, androgens, and estrogens have all been shown to have a marked effect on growth (5,27,34). These experimental situations are clinically paralleled by the well-known growth abnormalities mentioned previously.…”