BACKGROUND: Ameloblastoma is a frequent odontogenic benign tumor characterized 
by local invasiveness, high risk of recurrence and occasional metastasis and 
malignant transformation. Matrix metalloproteinase-2 (MMP-2) promotes tumor 
invasion and progression by destroying the extracellular matrix (ECM) and 
basement membrane. For this proteolytic activity, the endogenous inhibitor is 
reversion-inducing cysteine rich protein with Kazal motifs (RECK). The aim of 
this study was to characterize the relationship between RECK and MMP-2 
expression and the clinical manifestation of ameloblastoma.
METHODS: Immunohistochemistry and reverse transcription-polymerase chain 
reaction (RT-PCR) were employed to detect the protein and mRNA expression of 
RECK and MMP-2 in keratocystic odontogenic tumor (KCOT), ameloblastoma and 
ameloblastic carcinoma.
RESULTS: RECK protein expression was significantly reduced in KCOT (87.5%), 
ameloblastoma (56.5%) and ameloblastic carcinoma (0%) (P < 0.01), and was 
significantly lower in recurrent ameloblastoma compared with primary 
ameloblastoma (P < 0.01), but did not differ by histological type of 
ameloblastoma. MMP-2 protein expression was significantly higher in 
ameloblastoma and ameloblastic carcinoma compared with KCOT (P < 0.01). RECK 
mRNA expression was significantly lower in ameloblastoma than in KCOT (P < 
0.01), lower in recurrent ameloblastoma than in primary ameloblastoma, and was 
negative in ameloblastic carcinoma. MMP-2 mRNA expression was significantly 
higher in ameloblastoma compared with KCOT (P < 0.01), but was no different in 
recurrent ameloblastoma versus primary ameloblastoma. RECK protein expression 
was negatively associated with MMP-2 protein expression in ameloblastoma (r = 
-0.431, P < 0.01).
CONCLUSION: Low or no RECK expression and increased MMP-2 expression may be 
associated with negative clinical findings in ameloblastoma. RECK may 
participate in the invasion, recurrence and malignant transformation of 
ameloblastoma by regulating MMP-2 at the post-transcriptional level.