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Related Concept Videos

Bone Remodeling01:40

Bone Remodeling

Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
Hormones and Bone Tissue01:17

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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
Skeleton and Calcium Homeostasis01:21

Skeleton and Calcium Homeostasis

Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
Synthesis and Functions of Calcitonin00:51

Synthesis and Functions of Calcitonin

Calcitonin, a vital polypeptide hormone, regulates calcium levels within body fluids. It is released by the parafollicular cells, also known as C cells, situated in the follicular epithelium of the thyroid gland. Calcitonin responds to fluctuations in blood calcium levels and the influence of gastrointestinal hormones like gastrin and cholecystokinin.
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The Parathyroid Glands00:59

The Parathyroid Glands

The two pairs of parathyroid glands embedded within the posterior surface of the thyroid gland are restricted by a dense capsule around them. These glands comprise two distinct cell populations—parathyroid oxyphil and parathyroid principal cells- pivotal in calcium homeostasis.
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Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation
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Direct maxacalcitol injection into hyperplastic parathyroids improves skeletal changes in secondary

K Shiizaki1, I Hatamura, S Negi

  • 1Division of Nephrology and Blood Purification Medicine, Wakayama Medical University, Wakayama, Japan. shiizaki@wakayama-med.ac.jp

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Summary

Direct maxacalcitol injection into parathyroid glands improved bone health in rats with secondary hyperparathyroidism. This treatment reduced parathyroid hormone levels and hyperplasia, reversing bone disease.

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Area of Science:

  • Nephrology and Endocrinology
  • Bone Biology and Mineral Metabolism

Background:

  • Secondary hyperparathyroidism (s-HPT) is a common complication of chronic kidney disease.
  • Current treatments for s-HPT face challenges with resistance, partly due to altered vitamin D receptor (VDR) and Ca-sensing receptor (CaSR) expression and parathyroid gland (PTG) hyperplasia.
  • Direct maxacalcitol injection into PTGs shows promise in addressing these underlying factors.

Purpose of the Study:

  • To evaluate the long-term effects of direct maxacalcitol injection into PTGs on bone histomorphology in advanced s-HPT.
  • To assess the impact of this treatment on PTG hyperplasia, VDR and CaSR expression, and serum parathyroid hormone (PTH) levels.

Main Methods:

  • A rat model of advanced s-HPT was established using five/six nephrectomy and a high-phosphorus, low-calcium diet.
  • Rats received either direct maxacalcitol injection into PTGs followed by intravenous administration (DI-OCT+IV-OCT), direct vehicle injection with IV-OCT, IV-OCT alone, or no treatment.
  • Serum PTH, PTG weight, VDR/CaSR expression, and bone histomorphometric parameters were analyzed.

Main Results:

  • The DI-OCT+IV-OCT group showed sustained reduction in serum intact-PTH levels.
  • Significant decreases in PTG weight and increased VDR and CaSR expression were observed in the DI-OCT+IV-OCT group.
  • Bone histomorphometric analysis revealed significant improvements in osteitis fibrosa in both cancellous and cortical bones in the DI-OCT+IV-OCT group.

Conclusions:

  • Direct maxacalcitol injection into PTGs, combined with intravenous administration, effectively controls PTH levels by reducing PTG hyperplasia.
  • This therapeutic approach successfully reverses osteitis fibrosa in advanced s-HPT.
  • The findings suggest a promising strategy for managing complex secondary hyperparathyroidism and its skeletal complications.