RESUMO
Maxillary molars were extracted unilaterally from 4 young male rats so as to leave the agonist mandibular molars in hypofunction. The mandibular molars on the opposite side of the mouth acted as controls. Three days later, the animals were killed by perfusion and all mandibular molars removed en bloc. After demineralization, each block was trimmed, prepared for electron microscopy and embedded in Epon. The Epon blocks were trimmed so as to comprise the middle-third of the buccal periodontal ligament of the mesio-buccal root of the first molar together with some cementum and alveolar bone as landmarks. Two light-gold sections were cut from each trimmed block and systematically photographed in the electron microscope. The photographs were analysed stereologically so as to quantitate phagocytosed collagen (ICC), cytoplasm (CC) and extracellular fibrillar collagen (ECC). The results for the hypofunctional and contralateral control ligaments were compared with each other and with earlier results from similar but untreated (baseline) animals. The results were expressed as mean values for ICC, CC and ECC, and as the ratios ICC/ECC (the fraction of extracellular collagen phagocytosed), ICC/CC (collagen phagocytic activity per unit cytoplasm) and CC/ECC (cell density per unit extracellular collagen fibril). Significant differences were found for all measurements except ICC/ECC which remained the same in the three states of the ligament. The hypofunctional ligaments had the lowest collagen phagocytic activity and the highest cell density, whereas the ligaments from the untreated animals had the highest collagen phagocytic activity and the lowest cell density. The values for the contralateral control ligaments were intermediate between those for the other two states of the ligament. There was also a significant loss of recognizable, extracellular fibrillar collagen in the hypofunctional ligament. It is suggested that this loss of ECC and its replacement by less organized, pre-fibrillar forms of collagen may be an important mechanism in tooth eruption.
