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Adalberto Mosqueda-Taylor

Publications and source records attributed to Adalberto Mosqueda-Taylor.

20 records · Page 2Linked to original sources
PubMedDate not supplied

[Odontogenic keratocyst in dentigerous position. A clinical case].

Cysts that may develop in the maxillo-mandibular region and adjacent tissues may be of odontogenic origin, non-odontogenic origin, pseudocysts, cysts associated with the maxillary sinus and those developed from the soft tissues. These may vary as to their histogenesis, frequency, behavior and treatment. This article presents the clinical case of an 18-year-old female patient with an initial radiographic diagnosis of dentigerous cyst, which after exploratory punction and surgical removal under general anesthesia yielded a final diagnosis of odontogenic keratocyst. The patient's evolution was satisfactory with a 2-year radiographic control, without evidence of recurrence.

Adolescent↗
PubMedDate not supplied

Analysis of p53 protein by PAb240, Ki-67 expression and human papillomavirus DNA detection in different types of odontogenic keratocyst.

OBJECTIVE: To investigate the possible association between alterations in the p53 system and human papillomavirus (HPV) infection in the etiology of odontogenic keratocysts (OKCs) and to study proliferation and epithelial maturation patterns by topographic analysis of Ki-67 expression. MATERIALS AND METHODS: Eighty-three OKC samples (29 cases associated with nevoid basal cell carcinoma syndrome, 29 solitary non-recurrent cases 20 solitary recurrent cases, and 5 chondroid keratocysts) were studied by immunohistochemistry to detect p53 protein (PAb 244) and Ki-67 (MIB-1) expression, and by PCR to detect HPV DNA. RESULTS: Twelve cases (14.6%) expressed p53 protein; no case showed the presence of HPV DNA; 9 cases (11%) presented with mild epithelial dysplasia. The suprabasal expression of Ki-67 was significantly more frequent than its basal expression (p < 0.001). p53 protein expression was significantly associated with the presence of epithelial dysplasia (p = 0.023). Ki-67 expression was not associated with OKC type, the presence of dysplasia, or p53 expression. CONCLUSION: HPVs do not participate in the etiology of OKC, and it appears unlikely that a p53 gene mutation mechanism plays a major role in the genesis of OKC. OKCs show proliferation and genuine maturation behavior reminiscent of benign neoplasms with local destructive capacity.

Basal Cell Carcinoma↗