title: Osteocyte apoptosis and osteoclast presence in chicken radii 0-4 days following osteotomy.
abstract: Osteocyte apoptosis caused by load-induced microdamage is followed by osteoclastic bone remodeling, and a causal link between apoptosis and repair has been suggested. The objectives of the present study were to use a chick model to examine the incidence of osteocyte apoptosis and the presence of osteoclasts during the first 96 hours following an osteotomy, prior to extensive callus mineralization. Osteotomies were performed on the right radii of 24 chicks at 23-24 days of age. The left radii served as controls. Radii were collected and processed at six time points following surgery (0, 12, 24, 48, 72, and 96 hours). Decalcified bone tissue sections were stained either for apoptosis using a modified TUNEL procedure or for tartrate-resistant acid phosphatase to identify osteoclasts in the intracortical and periosteal envelopes. The percentage of apoptotic osteocytes, as well as osteoclast counts (n/mm or n/mm2) were quantified in four regions (0-1, 1-2, 2-4, and 4-8 mm from the site of the osteotomy; regions 1-4, respectively) in the osteotomized radii and in the same measured areas in the control radii. Data for osteocyte apoptosis and osteoclasts in the control limb were subtracted from the osteotomized limb data to identify differences due to surgical influence. The incidence of osteocyte apoptosis was significantly higher at 12, 24, 48, and 72 hours versus 0 hours following osteotomy, and the response was highest in region 1; however, there was no interaction between time and region. Intracortical osteoclast counts (n/mm2) were elevated after 48 hours, and the response was similar in all regions. The data demonstrate that osteocyte apoptosis occurs within 24 hours in response to an osteotomy and temporally precedes an increase in osteoclast presence. Hence, osteocyte apoptosis may play a role in signaling during the bone healing process.
authors.affiliation: Department of Animal Sciences, College of Agriculture and Life Sciences, University of Wisconsin, Madison, WI, USA.
authors.forename: W D
authors.initials: WD
authors.lastname: Clark
authors.forename: E L
authors.initials: EL
authors.lastname: Smith
authors.forename: K A
authors.initials: KA
authors.lastname: Linn
authors.forename: J R
authors.initials: JR
authors.lastname: Paul-Murphy
authors.forename: P
authors.initials: P
authors.lastname: Muir
authors.forename: M E
authors.initials: ME
authors.lastname: Cook
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002645:Chickens; D004195:Disease Models, Animal; D017102:Fracture Healing / Q000502:physiology; D020287:In Situ Nick-End Labeling; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D010010:Osteoclasts / Q000166:cytology* / Q000502:physiology; D010011:Osteocytes / Q000166:cytology* / Q000502:physiology; D010012:Osteogenesis / Q000502:physiology; D010027:Osteotomy; D011884:Radius / Q000166:cytology* / Q000601:surgery; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D007527:Isoenzymes; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase