title: Morphometric analysis of cortical bone upon the exposure to sustained delivery of anabolic promoting agents using adult male rats as a model.
abstract: Several investigations have documented that the use of anabolic agents could promote osteogenesis and enhance bone ingrowth in traumatized bone. Previously, anabolic steroids have been shown to increase the mineralization of bone. However, their clinical use has been limited because of the unwanted virilizing activity. The previous studies used systemic administration of anabolic steroids, which subjects other tissues within the body to high concentrations of hormones. In addition, different anabolic/androgenic steroids have varying affinities to different cell types within tissues. The specific objectives of this study were (i) to histopathologically evaluate the structural changes associated with sustained delivery of testosterone (T), dihydrotestosterone (DHT), and androstendione (AED) using adult male rats as a model, and (ii) to morphometrically evaluate the cortical areas and length upon the exposure of the aforementioned hormones for 90 days. A total of 23 adult rats were randomly divided into five groups (group I = control, group II = sham, group III = AED, Group IV = T and group V = DHT treated). At the end of the treatments the animals were euthanized and the x-rays, blood, and bones were analyzed using standard laboratory protocols. Data obtained from this investigation revealed the following: (A) all treated femurs appeared healthy with no traumatic responses observed in comparison to control animals, (B) measurements of the inner perimeter of the bone on the endosteal side showed significant reduction in the androgen treated animals. This suggesting that the androgens caused increases in the cortical bone. The differences seen in the amount of reduction was in the following ease: T > DHT > AED. C) quantitative measurements of the cortical length showed slight increases in the cortical lengths in the androgen treated rats in comparison to the control.
authors.affiliation: University of Mississippi Medical Center, Jackson, MS 39216, USA.
authors.forename: J
authors.initials: J
authors.lastname: Tramontana
authors.forename: H
authors.initials: H
authors.lastname: Benghuzzi
authors.forename: M
authors.initials: M
authors.lastname: Tucci
authors.forename: A
authors.initials: A
authors.lastname: Tsao
authors.forename: J
authors.initials: J
authors.lastname: Hughes
mesh_terms: D045930:Anabolic Agents / Q000494:pharmacology*; D000735:Androstenedione / Q000008:administration & dosage; D000818:Animals; D001842:Bone and Bones / Q000187:drug effects*; D002130:Calcium Phosphates; D002516:Ceramics; D013196:Dihydrotestosterone / Q000008:administration & dosage; D016503:Drug Delivery Systems; D004343:Drug Implants; D005264:Femoral Fractures / Q000188:drug therapy / Q000473:pathology; D017102:Fracture Healing / Q000187:drug effects*; D008239:Lysine; D008297:Male; D009929:Organ Size / Q000187:drug effects; D010012:Osteogenesis / Q000187:drug effects; D010710:Phosphates; D051381:Rats; D017207:Rats, Sprague-Dawley; D013739:Testosterone / Q000008:administration & dosage*
chemical_list: D045930:Anabolic Agents; D002130:Calcium Phosphates; D004343:Drug Implants; D010710:Phosphates; C112656:tricalcium phosphate lysine; D013196:Dihydrotestosterone; D013739:Testosterone; D000735:Androstenedione; D008239:Lysine