Objective: To evaluate the effect of proliferation and apoptosis of parathyroid cell in rabbits with primary hyperparathyroidism (PHPT).
Methods: A total of 80 adult Chinese rabbits were randomly divided into two groups (n = 40 each). The control group was fed with a normal diet (Ca: P, 1:0.7) while the experimental group a high phosphate diet (Ca: P,1:7) for 3-, 4-, 5-, or 6-month intervals to establish the animal model of PHPT. The parathyroid was totally removed for pathological examination after all rabbits were sacrificed. The thyroparathyroid complex was removed en bloc, fixed in neutral formalin and prepared for histological examination. The number of parathyroid cell in PHPT was calculated. Proliferation was determined by immunohistochemistry of proliferation cell nuclear antigen (PCNA) while apoptosis assessed by in situ dUTP biotin nick-end labeling (TUNEL).
Results: The number of parathyroid cell was 1.61 times in PHPT than that in the normal control (673 +/- 151, 418 +/- 25, t = - 12.112, P < 0.01). Apoptotic index (AI) increased significantly more in PHPT than that in normal control (200.2 per thousand +/- 125.6 per thousand, 11.0 per thousand +/- 3.0 per thousand, t = -10.193, P < 0.01). The rate of PCNA positive-cell increased significantly more in PHPT than that in control (50.5 per thousand +/- 11.6 per thousand, 26.7 per thousand +/- 2.8 per thousand, t = -13.120, P < 0.05). So did Bcl-2 (460 per thousand +/- 190 per thousand, 67 per thousand +/- 4 per thousand, t = -14. 120, P < 0.05). There was a positive correlation between AI and PCNA (r = 0.861, P < 0.05). It was the same as between AI and Bcl-2 (r = 0.871, P < 0.05). The value of bone mineral density decreased significantly more in PHPT than that in normal control (152 +/- 34, 189 +/- 12, t = 9.236, P < 0.05).
Conclusion: PHPT may be mainly induced by an excessive proliferation of parathyroid cells and an acceleration of apoptotic process.