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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.

Diffuse parenchymal lung diseases (DPLD) represent a diverse group of disorders affecting the distal lung parenchyma, specifically the tissue and spaces surrounding the alveoli, which may be filled with inflammatory cells, proliferating fibroblasts or established fibrosis, often leading to architectural distortion and impaired gas exchange. While the underlying pathogenetic mechanisms are known or inferred for some DPLD (such as sarcoidosis, silicosis, drug reactions and collagen vascular diseases), the pathogenesis of the majority of these entities - particularly those characterized by progressive fibrosis - is poorly understood. Several lines of evidence indicate that the development of pulmonary fibrosis is genetically determined. They include: 1. familial clustering; 2. the occurrence of pulmonary fibrosis in the context of rare inherited disorders; 3. substantial variability in the development of pulmonary fibrosis amongst individuals exposed to organic or inorganic dusts; 4. difference in susceptibility to fibrogenic stimuli amongst inbred strains of mice. This review focuses on idiopathic pulmonary fibrosis (IPF) and sarcoidosis, the two most common DPLD and the two entities for which there is stronger evidence of a genetic predisposition, although how aberrant genes interact with each other and with environmental factors, such as smoking in IPF and infectious agents in sarcoidosis, in determining disease susceptibility and clinical phenotypes is largely unknown. Finally, we discuss practical issues and implications for both patients and physicians of recent advances in the genetics of sarcoidosis and IPF.