An analysis of the prevalence of peripheral giant cell granuloma and pyogenic granuloma in relation to a dental implant.

BACKGROUND: The aim of the present investigation was to evaluate the literature recurrence of peripheral giant cell granuloma and pyogenic granuloma associated with dental implants. It's important to know the characteristics present in these lesions and possible effects on the prognosis of dental implants. METHODS: An electronic search without time restrictions was done in the databases: PubMed/Medline. With the keywords "Granuloma" OR "Granuloma, Giant Cell" OR "peripheral giant cell" OR "Granuloma, Pyogenic" AND "Dental implants" OR "Oral implants". RESULTS: After applying the inclusion and exclusion criteria, a total of 20 articles were included, which reported 32 lesions (10 pyogenic granulomas, 21 peripheral giant cell granulomas and one peripheral giant cell granuloma combined with peripheral ossifying fibroma, all associated with implants). According to our review, these lesions are more frequent in males and in the posterior region of the mandible. Both excision and curettage of the lesion, compared to only excision, presented similar recurrences (40%). Explantation of the implant was performed in 41% of cases without additional recurrences. The results are not statistically significant when comparing one lesion to the other in terms of explantation (p = 0.97), recurrence (p = 0.57) or bone loss (p = 0.67). CONCLUSIONS: The main therapeutic approach is tissue excision. The lesions show a high recurrence rate (34.4%), which often requires explantation of the associated implant. This recurrence rate is not affected by curettage after excision.

Quantification of inflammatory, angiogenic, and fibrous components of reactive oral lesions with an insight into the pathogenesis.

Background: Reactive oral lesions pose diagnostic difficulties as they mimic each other clinically. A definitive diagnosis is made based on the histopathological presentation of this group of lesion. Stromal microenvironment is the key to the sequence of the stages of these lesions. Stringent quantification of each component of the stroma is important to understand the pathogenesis. The aim is to evaluate inflammation, angiogenesis, and fibrosis in the reactive group of lesions through quantitative analysis. Materials and Methods: Blocks of irritation fibroma, inflammatory fibrous hyperplasia, pyogenic granuloma, and normal mucosa were retrieved from the archives and Hematoxylin and Eosin (H&E) and Masson Trichrome staining were done. The severity of inflammation, epithelial thickness, collagen proportionate area, integrated density of collagen, Mean Vascular Area (MVA), Mean Vascular Perimeter (MVP), and Mean blood vessel percentage area (MBVPA) were analysed quantitatively using Image J software version 1.8. The pattern of rete ridges at the epithelium-connective tissue interface was analysed qualitatively. Results: Inflammatory fibrous hyperplasia presented with severe inflammation (60%). Mean Vascular Percentage Area (MVPA) and Mean Vascular Perimeter (MVP) were increased in pyogenic granuloma. The mean collagen proportionate area and the integrated density of collagen were found to be more in irritation fibroma (64.47%, 2519638.01 ± 810471.58 µm2). The epithelial thickness was highest in inflammatory fibrous hyperplasia (62.71 ± 18.86 µm). Conclusion: Reactive oral lesions are histologically distinct, yet they exhibit considerable overlap depending on the stage of the lesion. A morphometric quantitative exploration of the individual pathogenic components may aid in specific diagnosis.

Comparative Evaluation of SMAD-2 Expression in Oral Submucous Fibrosis and Reactive Oral Lesions.

BACKGROUND: The event of fibrosis encompasses involvement of definite immunological and molecular mechanisms. As quite a lot of pro-fibrotic pathways are concerned, a multipronged approach is obligatory to cognize the fibrotic events. SMAD signaling pathway hasn't been studied oral fibrotic events.In the progression of cramming the SMAD signaling pathway in OSMF, the first initiator protein of the pathway was considered for evaluation in the present study. MATERIALS AND METHODS: A total of 100 subjects consisting of 20 controls, 40 patients with reactive lesions such as Traumatic Fibroma, Epulis Fissuratum and Gingival Hyperplasia and 40 patients with Oral Submucous Fibrosis were recruited for the study. Tissue homogenates were assayed by quantitative sandwich enzyme immunoassay technique using Human Mothers Against Decapentaplegic Homolog 2 (Smad2). RESULTS: SMAD 2 expression values showed significant difference between control and OSMF group. However, the difference between reactive lesions with control and OSMF were not statistically significant. CONCLUSION: Graded increase of SMAD 2 expression from control,reactive lesions and OSMF were observed accentuating the role of SMAD signalling pathway in fibro genesis. Further this can be validated to generate effective antifibrotic targets.