Mast cell‐derived tryptase in odontogenic cysts

Abstract

Inflammatory and developmental cysts of the jaws are relatively common bone destructive lesions in the human maxillofacial skeleton but their pathogenesis is still poorly understood. In this study the role of mast cells (MC), and mast cell tryptase in particular, was evaluated in the pathophysiology of bone resorption and jaw cyst formation in different types of cysts. The distribution of MC and the amount of tryptase in histological tissue sections were determined by immunohistochemistry using monoclonal antihuman tryptase antibodies and the results were quantitated by using an image analyzing system. The amount of tryptase was further studied by Western-blotting and measurement of trypsin-like activity from the neutral salt extracts obtained from different types of jaw cysts. In contrast to control tissue, high trypsin-like activities and abundant immunoreactive tryptase were observed in the extracts of all types of cysts studied (radicular, dentigerous and keratocyst). In tissue sections the highest amount of tryptase-positive staining was observed in radicular cysts (mean 6.2% of reference area) and the lowest amount in keratocysts (mean 2.1% of reference area, P < 0.01). MC were found to be located in inflammatory cell-rich tissue areas and just beneath the cyst epithelium. Importantly, MC located at the border of bone were observed to be degranulated, indicating high activity of MC and release of tryptase at the regions of early bone destruction. Based on previous findings addressing the role of mast cell tryptase in proteolytic cascades, and the known association of MC with osteoporosis, we suggest that mast cells and mast cell tryptase may contribute significantly to jaw cyst tissue remodelling during growth of a cyst, and to the destruction of the surrounding bone, resulting in jaw cyst expansion.

Comparison of Mast Cells and Inflammatory Cells within Periapical Lesions and Comparison of Degranulated Mast Cells Between Fibrous and Inflamed Area in Radicular Cysts: An Immunohistochemical Study

“…Furthermore, in systemic mastocytosis, which is characterized by an abnormal proliferation of mast cells, approximately 60-70% of the patients develop radiographically detectable lesions. Inhibition of mast cell mediator release with ketotifen was shown in one case to lead to reversal of bone changes [13]. So, more number of degranulated mast cells in the cyst group suggests more resorption of the bone and hence expansion of the lesion.…”

Correlation between inflammatory infiltrate and epithelial lining in 214 cases of periapical cysts

“…9 The inflammatory infiltrate in the cystic lining appears to play an important role in the pathogenesis of periapical cysts. 10 Therefore, the purposes of the present study were to evaluate the prevalence of periapical cysts, identify their clinical and microscopic features and correlate their microscopic features with the inflammatory infiltrate present in the lesion.…”

Analysis of the presence and location of mast cells in periapical cysts and periapical granulomas

“…The authors stated that the constituents of the periapical capsule included mast cells, among other cell types. This specific location could emphasize the findings reported in 1996, concerning bone resorption, in the work of Teronen et al 20 . These authors stated that mast cells, typically those belonging to the degranulated variety, were located in the periphery of odontogenic cysts and used the secretion of tryptase to contribute to bone resorption during the growth of cysts.…”

“…This can only be described as an anti-inflammatory action which restrains the excess inflammation. They also promote neutrophil and eosinophil aggregation, while stimulate T lymphocyte and influence the endothelial cells to release mediators upon activation, contributing during process of repair by neo-angiogenesis, fibrinogenesis and reepithelization, characterizing a pro inflammatory action as well 20 . Therefore, depending on the situation, mast cells can stimulate inflammation or restrain it, influencing the acutization and chronification processes.…”