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Home | Pregnancy Timeline | News Alerts | News Archive June 7, 2013

 
Bone reversal cells

Reversal cells actually cover more than 80 percent of the resorbed bone surfaces. Using histomorphometry and immunohistochemistry on human bone biopsies, researchers found that the reversal cells colonizing the resorbed bone surfaces are immature osteoblastic cells which gradually mature into bone forming osteoblasts during the reversal phase, and prepare the bone surface for bone formation.

Credit: The American Journal of Pathology (Andersen et al.)







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Reversal cells balance bone formation and reabsorption

In adults, bones are maintained and kept healthy by constant remodeling. This consists of bone reabsorption and formation by osteoblast cells. If the delicate balance between these two processes fails, osteoporosis or other bone disorders develop. Research is just beginning to understand how these two functions work together.

Analyzing biopsy tissue from patients with postmenopausal osteoporosis—occurring after menopause—and primary hyperparathyroidism*, investigators have begun to pay increasing attention to "reversal cells." These cells appear before bone formation and during bone remodeling.


The hope is that reversal cells will someday become therapy targets in the prevention of osteoporosis and other bone disorders.

"Reversal cells may represent the missing link necessary to understand coupling between bone resorption and formation and to prevent osteoporosis."

Jean-Marie Delaisse, PhD, professor Clinical Cell Biology, Institute of Regional Health Services Research, University of Southern Denmark and Vejle-Lillebaelt Hospital in Vejle


This study is published in the July 2013 issue of The American Journal of Pathology.

Reversal cells actually cover more than 80% of resorbed bone surface. Using histomorphometry and immunohistochemistry on human bone biopsies, researchers found that reversal cells colonizing the resorbed bone surfaces are immature osteoblastic cells, which gradually mature into bone forming osteoblasts during the reversal phase, and prepare the bone surface for bone formation.

Researchers also found that some reversal cells display characteristics suggesting an "arrested" physiological status. These arrested reversal cells showed no physical connection with the bone forming surface, reflect reduced cellular density, and a reduced expression of osteoblast markers.


Biopsies from postmenopausal patients with osteoporosis showed a high proportion of arrested cells, but no such cells were found in biopsies from patients with primary hyperparathyroidism, where transition between bone resorption and formation occurs optimally.

Negative correlations were found between the proportion of arrested cells in biopsies from patients with osteoporosis and bone formation parameters.

In other words, larger arrested cell surfaces were associated with bone loss. Other findings suggest that the reversal phase is longer in those patients with postmenopausal osteoporosis compared to those with primary hyperparathyroidism.


Investigators describe three concurrent types of bone remodeling cycles. Their respective prevalence depends on the pathophysiology of the situation. All bone remodeling processes start with bone resorption, but differ by the degree of restitution of the bone matrix:

  • In coupled and balanced bone remodeling, the bone matrix is completely restored which is primarily seen in healthy and primary hyperparathyroid bone.
  • In coupled and unbalanced bone remodeling, bone formation occurs, but the resorbed cavity is not completely restored.
  • In uncoupled bone remodeling, the resorbed cavity remains completely unfilled— an arrest of the reversal phase—with no new bone formation.

Coupled and unbalanced bone remodeling and uncoupled bone remodeling both appear to contribute to bone loss in osteoporosis.

"Our observations suggest that arrested reversal cells reflect aborted remodeling cycles which did not progress to the bone formation step," says Dr. Delaisse. "We therefore propose that bone loss in postmenopausal osteoporosis does not only result from a failure of bone formation as commonly believed, leading to incomplete filling of resorption cavities, but also from a failure at the reversal phase, uncoupling bone formation from reabsorption."

*Hyperparathyroidism is overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH). The parathyroid hormone regulates calcium and phosphate levels and helps to maintain these levels. Excessive PTH secretion may be due to problems in the glands themselves, in which case it is referred to as primary hyperparathyroidism and which leads to hypercalcaemia (raised calcium levels). It may also occur in response to low calcium levels, as encountered in various situations such as vitamin D deficiency or chronic kidney disease; this is referred to as secondary hyperparathyroidism. In all cases, the raised PTH levels are harmful to bone, and treatment is often needed.

http://dx.doi.org/10.1016/j.ajpath.2013.03.006

Original article: http://www.eurekalert.org/pub_releases/2013-06/ehs-rcm060413.php