Abstract
Immunostaining revealed the presence of KLK 3, 4, 9 & 11 in all tissue types studied. KLK 5 was present only in KOT’s (p<0.001). Greater KLK 3 staining was present in ameloblastomas (p<0.01) and KOTs (p<0.05) than in the odontogenic control. KLK 9 exhibited greater staining in KOTs (p<0.05) and dentigerous cysts (p<0.05) than the odontogenic control. KLK 11 had greater staining in the ameloblastomas (p<0.05) than in non-odontogenic cystic controls. Expression of KLK 1, 4, 7, 8, 10 & 12 mRNA was found in pooled ameloblastoma tissue. Expression of KLK 7 and 10 mRNA was greater than that of KLK 1, 4, 8 & 12 in the ameloblastoma tissue. KLK 2, 3, 5, 6, 9, 11, 13, 14 & 15 mRNA were not identified in ameloblastoma tissue. For the first time, KLK 3, 4, 5, 9 & 11 have been identified in maxillofacial cysts and tumours. KLK 3 is present in significantly greater amounts in benign neoplasms of odontogenic origin, the ameloblastoma and KOT, when compared to the odontogenic hamartoma. KLK 11 is present in significantly greater amounts in the benign neoplasm (ameloblastoma) compared to non-odontogenic cystic control (nasopalatine duct cyst). Interestingly, KLK 3 and 11 mRNA was not identified in the ameloblastoma using RTPCR, suggesting that KLK 3 and 11 protein may be recruited, sequestered or have a long half life in benign neoplasms of odontogenic origin. As expected, KLK 5, which is known to be involved in the process of keratinization, is present only in the KOT. Identification of KLK 4 mRNA in ameloblastoma tissue was also expected; it is implicated in normal amelogenesis. With further investigation, it may be possible to use KLK’s as biomarkers for identifying and monitoring these lesions. Additionally, if the physiologic role of KLK’s in neoplasia can be identified, they may provide a target for minimally invasive therapeutics.
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