The expression pattern of collagen I in irradiated mandibular salivary glands of rats

UNLABELLED: Irradiation damage to salivary glands leads to loss of function and fibrosis. Immunohistochemical analysis of extracellular matrix proteins might give a more precise insight into the irradiation damage of glands. Collagen I (C-I) is a major component of the extracellular space. The aim of this study was to analyse the effects of irradiation on the distribution pattern of C-I in the salivary glands of rats.

MATERIALS AND METHODS: Sixty female Wistar rats were fractionated irradiated up to 60 Gy (left side of the neck; 2 Gy/d, 5d/week; total dosage either 20, 40 or 60 Gy). The glands were explanted after 6 or 12 months following supravital anesthesia, the shielded right gland serving as internal control. C-I was detected immunohistochemically.

RESULTS: In non-irradiated animals the immunoreaction was mainly homogeneous and slight around the ductal epithelia, in the area of the capsule and septae and the peri- and epineurium of nerves. A statistically significant difference was identified in the irradiated rats vs control animals and comparing in-the-radiation field (left side) vs outside-the-radiation field (right side) situated glands. Multivariate analysis revealed a statistically significant increase in staining of irradiated rats concerning the excretory ducts, the area of the capsule and septae, the nerves and striated ducts and adventitia of vessels [p = 0.0001]. The increase of immunoreaction in irradiated glands started above 20 Gy total dosage and was at its maximum after 60 Gy. However, the expression profile was inhomogenous following 20 Gy exposure and did not differ statistically from glands of control animals. Neither the age of the animals nor the latency period following exposure to the radiation source yielded a statistically significant effect on the immunoreaction.

CONCLUSION: Studies on irradiation damage to the salivary glands require a more detailed description of the proteins accumulating in the extracellular space, thereby forming the so-called "fibrosis". These accumulations of proteins, e.g. C-I, may both support apoptosis and support a hypoxic environment giving rise to transformed cells.