Multiple idiopathic external cervical root resorption in patient treated continuously with denosumab: a case report.

BACKGROUND: External root resorption is an irreversible loss of dental hard tissue as a result of odontoclastic action. Multiple external cervical root resorptions in permanent teeth are rare. The exact cause of external cervical root resorption is unclear. It is currently well established that RANK/RANKL signaling is essential for osteoclastogenesis and osteoclast-mediated bone resorption. Denosumab is an anti-RANKL antibody used for the treatment of postmenopausal osteoporosis. RANK/RANKL pathway suppression by denosumab is expected to suppress the activity of clastic cells responsible for hard tissue resorption involving both osteoclasts and odontoclasts. CASE PRESENTATION: This case report demonstrates aggressive and generalized idiopathic external cervical root resorption that started and advanced during ongoing antiresorptive therapy with the human monoclonal RANKL-blocking antibody denosumab without discontinuation of therapy in a 74-year-old female patient treated for postmenopausal osteoporosis. The extent of resorptive defects was too large and progressively led to fractures of the teeth. The number of teeth involved and the extend of destruction excluded conservative treatment. The affected teeth had to be extracted for functional prosthetic reconstruction. CONCLUSIONS: This finding suggests that treatment with denosumab may be associated with severe and aggressive odontoclastic resorption of multiple dental roots despite an adequate inhibitory effect on osteoclasts in the treatment of osteoporosis. The RANKL-independent pathways of clastic cell formation are likely to be involved in this pathological process.

Gossypiboma mimicking recurrent mandibular tumor: case report.

Gossypiboma is not a commonly known surgical complication. It is a tumorous lesion usually caused by hemostatic material used in surgery. Such lesions are most commonly described after abdominal surgery. In this case report, the authors describe a case of a 17 year old female patient, operated for a mandible tumor. Histopathologically it was an ameloblastoma. The patient was treated lege artis, with the use of Surgicel® felt (Surgicel FibrillarTM Absorbable Hemostat). After two months, the young woman returned to clinics with a tumorous lesion at the same location. On the CT scan the lesion appeared to be a recurrence of the originally diagnosed ameloblastoma. Histopathologically, the lesion consisted of a foreign material with surrounding granulation tissue and massive inflamation. The foreign material had an atypical structure. Subsequent consultations and consensus at the clinic confirmed that it was a haemostatic foreign material with a surrounding hyper-inflammatory response mimicking a tumor, known in the literature under various names, most often as gossypiboma or textiloma.

Intracellular signaling MAPK pathway after cerebral ischemia-reperfusion injury.

The MAPK/ERK/p38 are signal transduction pathways that couple intracellular responses to the external stimuli. Contrary to ERK protein which is part of the survival route, presence of p38 could have an impact on cell injury. Tolerance induced by ischemic preconditioning (IPC) is a phenomenon of tissue adaptation, which results in increased tolerance to lethal ischemia-reperfusion injury (IRI). Paper describes changes in MAPK protein pathways after brain IPC. Ischemia was induced by 4-vessels occlusion and rats were preconditioned by sub-lethal ischemia. Western blot and immunohistochemistry identified ERK/p38 proteins in injured areas. The highest level of the pERK was detected at 24 h in IPC groups. A contrary pattern of MAPK/p38 activation was observed in this group, where the lowest level of p38 was displayed at 24 h after ischemia. This suggests that the MAPK signal transduction might have a potential role in tissues response subjected to IRI and in the phenomenon of tolerance.