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Amgen Bone Health Mentoring Program

Monday, October 15, at 11:30am – 2:30pm ◼ Ruth Chris, Minneapolis, MN

1038 PTH/PTHrP Receptor Signaling in Osteocytes

Regulates Anabolic and Catabolic Bone Responses to

PTH by Modulating Bone Remodeling via Sclerostin and

RANKL Expression.

Saini V, Fulzele K, Barry K, et al.
Session: Concurrent Oral Session 07: Osteocytes ◼
Weekday, October 13, 02:30 PM - 02:45 PM ◼ Room

101C/Minneapolis Convention Center

Results Abstract Information Additional Notes from
Poster/Presentation*
Conclusions ▪ Intermittent PTH-related higher cortical
Implications thickness, bone area and continuous Updated/Additional
for Canadian PTH-mediated decreases in bone Data, Key Takeaways
volume, trabecular number and spacing
Practice as noted in the control mice were not
seen in OcyPPRKO mice.

▪ Immunohistochemistry revealed
increased Sclerostin and decreased
RANKL expression in osteocytes of
OcyPPRKO as compared to controls.

▪ PTH induced a significant reduction in the
number of multinucleated osteoclasts in
OcyPPRKO co-culture as compared to
controls. (p<0.05).

▪ Osteoprotegrin treatment completely
abrogated osteoclast formation in both
groups indicating that PPR signaling in
osteocytes regulates osteoclastogenesis
via a RANKL-mediated pathway.

▪ PPR on osteocytes regulates RANKL
expression, which in turn regulates
osteoclast formation and bone
remodeling.

Discussion Points, Key Takeaways