gms | German Medical Science

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2016)

25.10. - 28.10.2016, Berlin

Hypochlorhydria-induced calcium malabsorption does not affect fracture healing but increases post-traumatic bone loss in the intact skeleton

Meeting Abstract

  • presenting/speaker Melanie Haffner-Luntzer - Institut für Unfallchirurgische Forschung und Biomechanik, Universität Ulm, Ulm, Germany
  • Aline Heilmann - Institut für Unfallchirurgische Forschung und Biomechanik, Universität Ulm, Ulm, Germany
  • Verena Heidler - Institut für Unfallchirurgische Forschung und Biomechanik, Universität Ulm, Ulm, Germany
  • Thorsten Schinke - Institut für Osteologie und Biomechanik, Hamburg, Germany
  • Michael Amling - Institut für Osteologie und Biomechanik, Hamburg, Germany
  • Timur Alexander Yorgan - Institut für Osteologie und Biomechanik, Hamburg, Germany
  • Annika vom Scheidt - Institut für Osteologie und Biomechanik, Hamburg, Germany
  • Anita Ignatius - Institut für Unfallchirurgische Forschung und Biomechanik, Universität Ulm, Ulm, Germany

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2016). Berlin, 25.-28.10.2016. Düsseldorf: German Medical Science GMS Publishing House; 2016. DocGR18-188

doi: 10.3205/16dkou462, urn:nbn:de:0183-16dkou4624

Veröffentlicht: 10. Oktober 2016

© 2016 Haffner-Luntzer et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Objectives: Efficient calcium absorption is essential for skeletal health. Patients with impaired gastric acidification display low bone mass and increased fracture risk, because calcium absorption is dependent on gastric pH (Chiu et al., 2010). Due to the increasing prevalence of patients suffering from low gastric acidification (Burge et al., 2007), it is of high clinical relevance to elucidate the effects of calcium malabsorption on fracture healing. Here we investigated fracture healing and post-traumatic bone turnover in mice deficient in Cckbr, encoding a gastrin receptor that affects acid secretion by parietal cells. Similar to patients with hypochlorhydria, Cckbr-/- mice display high gastic pH, calcium malabsorption and osteopenia (Schinke et al., 2009). Furthermore, we studied the effects of calcium gluconate supplementation after fracture in these mice.

Methods: Cckbr-/- and wildtype (WT) mice received a femur osteotomy stabilized by an external fixator and were fed either a standard or calcium gluconate-enriched diet, because of the greater solubility of calcium gluconate at neutral pH than other calcium conjugates. Healed and intact bones were assessed at day 24 and 32 after fracture by biomechanical testing, histomorphometry, micro computed tomography and quantitative backscattering. Parathyroid hormone (PTH) serum levels were determined by ELISA at day 0, 10, 24 and 32 after fracture. Statistical analysis: Kruskal-Wallis test, p<0.05, n=5-12.

Results and Conclusion: Notably, we found that fracture healing was unaffected in Cckbr-/- mice. However, Cckbr-/- mice displayed increased calcium mobilization from the intact skeleton during bone healing, confirmed by significantly elevated PTH levels (+36%) and osteoclast numbers (+38%) compared to WT mice at day 24 after fracture. Also in WT mice, we found elevated levels of PTH in the serum after fracture (80 pg/ml pre-OP vs. 280 pg/ml 24 days post-OP), indicating that the normal standard mouse diet did not supply the calcium needs for fracture healing. Calcium supplementation significantly reduced secondary hyperparathyroidism and bone resorption in the intact skeleton in both genotypes, but more efficiently in WT mice. Furthermore, calcium administration improved bone healing in WT mice, indicated by significantly increased bending stiffness (+66%), bone mineral density (+20%) and calcium content of the fracture callus (+14%), whereas it had no significant effect on fracture healing in Cckbr-/- mice.

We conclude that under conditions of hypochlorhydria-induced calcium malabsorption, calcium, which is essential for callus mineralization, appears to be increasingly mobilized from the intact skeleton in favor of fracture healing. Calcium supplementation during fracture healing prevented systemic calcium mobilization, thereby maintaining bone mass and improving fracture healing in healthy individuals whereas the effect was limited by gastric hypochlorhydria.