Peripheral giant cell granuloma associated with a dental implant.

BACKGROUND: Peripheral giant cell granuloma (PGCG) is an uncommon pathology that affects gingival or alveolar mucosa. Although PGCG can be associated with dental implants, little is known about this lesion and implant osseointegration as well as its etiopathogenesis and the treatments available. This study sought to report a rare case of PGCG associated with dental implant, emphasizing its clinical and histopathological aspects. CASE PRESENTATION: A 53-year-old man had an exophytic, reddish lesion, around a crown attached to a dental implant located in the left mandible. Radiographically, there was bone loss around the implant. After excisional biopsy, histological examination revealed a submucosal proliferation of multinucleated giant cells rendering the diagnosis of peripheral giant cell granuloma. Patient has been under follow-up for 6 months with no recurrence. CONCLUSIONS: Peri-implant lesions must be completely removed to prevent recurrence of PGCG and implant failure, even in cases suspected to be reactive. Besides, histological examination must be performed on all peri-implant reactions to achieve the appropriate diagnosis and, consequently, the best treatment and follow up.

Kidney osteoclast factors and matrix metalloproteinase expression in a mice model of diet-induced obesity and diabetes.

The role of RANKL/RANK/OPG system on bone remodeling is well known, and there is evidence that it is also important to cardiovascular and kidney pathology, although the underlying mechanisms are not elucidated so far. Thus, we investigated in a mice model of diet-induced obesity and diabetes if renal histopathological changes are associated with the expression of RANKL/RANK/OPG system and matrix metalloproteinases (MMPs). Three months old C57BL/6 mice were fed with control (C) AIN93 M diet or high-fat high sucrose (HFHS) diets for 21 weeks (CEUA/UFF #647/15). The two groups presented weight gain, but it was higher in the HFHS group compared to the C group (+35%, P = 0.0001). The HFHS group also had increased epididymal, inguinal and retroperitoneal fat pad weight (+121%, P = 0.0006; +287%, P = 0.0007 and; +286%, P < 0.0001, respectively), and hyperglycemia (+43%, P = 0.02). The kidney of some HFHS fed mice displayed mononuclear inflammatory cell infiltrate (40%), perivascular fibrosis (20%), and focal tubule mineralization (20%). Glomeruli hypertrophy was not detected. Unexpectedly, OPG, RANK, MMP-2, and MMP-9 expression was not altered in HFHS groups (Western blot analysis). In conclusion, the expression of RANKL/RANK/OPG system proteins and MMPs was not influenced by diet-induced obesity and diabetes in the kidney of male C57BL/6 mice, although some adverse histopathological remodeling is noticed in the renal tissue.

Synchronous orofacial granulomatosis and mucoepidermoid carcinoma: paraneoplastic syndrome or coincidence?

Some malignant neoplasias induce the appearance of local or systemic manifestations at distant sites, which can act as indicators of their presence in a process named paraneoplastic syndrome. Granulomatous reactions have already been described related to malignancies. This report describes a case of synchronous orofacial granulomatosis and mucoepidermoid carcinoma and discusses the significance of this association.

Rhinoliths causing palatal perforation: case report and literature review.

Rhinoliths are calcified masses formed within the nasal cavity because of the solidification of mucus, debris, or foreign objects by gradual accretion of mineral salts. They are mostly asymptomatic and incidentally diagnosed, although some patients may complain of nasal discharge and obstruction. Ulceration of the nasal mucosa, facial swelling, and bone destruction are less frequently observed but bring about difficulties for differential diagnoses with several pathologic entities. This article presents a case of a 54-year-old woman with a rhinolith causing palatal perforation, focusing on the diagnostic process and histopathologic characteristics.