Osteonecrosis maxilar asociada a infección por Actinomyces y tratamiento con bifosfonatos / Actinomyces and bisphosphonate-related osteonecrosis of the jaw

Objetivo. Describir anatomopatológicamente la osteonecrosis maxilar asociada a tratamiento con bifosfonatos y su asociación con infección por Actinomyces spp. Material y método. Se seleccionaron casos con diagnóstico clinicopatológico de necrosis maxilar o mandibular en las bases de datos de los hospitales de La Paz y de Guadalajara. Resultados. Se hallaron 16 casos con constatación anatomopatológica de necrosis ósea maxilomandibular e infección por Actinomyces. En 13 casos se informó de tratamiento con bifosfonatos. Un caso correspondió a osteorradionecrosis infectada. En 2 casos no se informó de tratamiento alguno. Conclusiones. Este cuadro es poco frecuente y suele sospecharse clínicamente, pero es relativamente desconocido para patólogos generales. Constantemente se asocia a infección por Actinomyces spp, que probablemente influya en la patogenia del proceso(AU)

Objetive. To describe pathological features in bisphosphonate-related osteonecrosis of the jaw and Actinomyces spp. infection. Materials and method. All cases, from both our hospitals, with a clinicopathological diagnosis of osteonecrosis of the jaw were reviewed. Results. Sixty cases of osteonecrosis of the jaw and Actinomyces infection are reported. Thirty cases were treated with bisphosphonate, 2 cases were untreated, and one case corresponded to infected osteoradionecrosis. Conclusion. This is a rare disease that is detected usually by clinicians but pathologists should be aware of it. It is constantly associated with, and probably caused by, Actinomyces spp. infection(AU)

Primary testicular lesions are associated with testicular germ cell tumors of adult men.

The present study aims to establish the nature and frequency of testicular lesions in the parenchyma adjacent to testicular germ cell tumors (TGCT) to improve understanding of the factors involved in the development of testicular cancer. Fifty-three cases of TGCT that were fixed in both neutral-buffered formalin and Bouin solution, allowing for the nuclear characterization of Sertoli cells (SCs), were included in this study. In each case, at least 3 sections of different areas of preserved parenchyma surrounding the TGCT were studied. We found Leydig cell hyperplasia, microlithiasis, angiopathy, adenomatous hyperplasia of the rete testis, SC nodules, SC dysgenesis and involution, SC-only tubules, tubular atrophy, adluminal compartment lesions, hypospermatogenesis associated with spermatocyte sloughing, spermatogonial maturation arrest, and hypertrophic and multinucleated spermatogonia. These lesions were found in regions both adjacent and far away from the tumoral mass, and abnormal seminiferous tubules were found intermingled with those showing complete spermatogenesis, suggesting that these lesions are primary and existed before the development of the tumor. Our study suggests that SCs might play a more important role in the development of testicular tumors than previously thought. Our data supports the hypothesis that there is an abnormal differentiation of SCs, caused either by genetic anomalies or by environmental agents during fetal life. This abnormal SC differentiation may cause not only primary spermatogenesis failure and spermatogenesis arrest at different levels, but may also contribute to the poor differentiation of gonocytes into spermatogonia. The abnormal gonocyte differentiation might favor the development of dysplastic germ cells that may later transform into intratubular germ cell neoplasia, unclassified type.