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Compensatory Hyperplasia of the Rat Submandibular Gland Following Unilateral Extirpation
D. Schwartz-Arad
Department of Anatomy and Embryology, Hebrew University-Hadassah Medical School, P.O.B. 1172, Jerusalem 91010, Israel
Y. Michaelp
Department of Anatomy and Embryology, Hebrew University-Hadassah Medical School, P.O.B. 1172, Jerusalem 91010, Israel
G. Zajicek
The Hubert H. Humphrey Center of Experimental Medicine and Cancer Research, Hebrew University-Hadassah Medical School, P.O.B. 1172, Jerusalem 91010, Israel
This study investigated the morphological changes in rat submandibular glands undergoing compensatory hyperplasia. Fifteen adult male rats underwent left submandibulectomy, after which they were killed in groups of five (at days 3,7, and 14), and their right submandibular glands (SMG) were excised. Fifteen control rats were killed in groups of five (at days 0, 7, and 14), and their right SMG were removed. Sections of 3 µm were cut, and the parenchymal and stromal cells were counted in 50 microscopic fields and sorted according to their morphological features and "class". Class is equivalent to the number of nuclei in an acinar or tubular cross-section.
No change in glandular weight was noted post-surgery. Total cell count/field rose to 138.5 ± 7.1% of control values on day 3 after gland extirpation, remaining almost constant thereafter until the end of the experiment. Acinar cell count and class showed a 154.1% peak on day 3, followed by a 30% drop in cell count by day 7 and an equivalent decline in class by day 14. Tubular cell count increased gradually to 146.5% by day 14, without a change in class. In the first week, the increase in tubular cells was mainly due to intercalated duct (ID) cells, while in the second week, there was a sharp rise in granular duct (GD) cells. This diverging cellular behavior indicates that the GD cell stems from the ID cell.
The cellular changes in the hyperplastic SMG indicate death of newly generated acinar cells and expansion of the glandular progenitor compartment, as expressed in elongation of the ID.
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Journal of Dental Research, Vol. 70, No. 10,
1328-1331 (1991)
DOI: 10.1177/00220345910700100301
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