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1 h, intrapulpal calcifications, and localized gingival hyperplasia.
2 osal bleeding and ulceration, petechiae, and gingival hyperplasia.
3 ingival tissue could provide a mechanism for gingival hyperplasia.
4 g amlodipine and determine the prevalence of gingival hyperplasia.
5 channel blockers are known to contribute to gingival hyperplasia.
6 hat amlodipine, 5 mg per day, did not induce gingival hyperplasia.
7 eered to undergo a screening examination for gingival hyperplasia.
8 lymphoproliferative disorders presenting as gingival hyperplasia.
10 eported immunosuppression-induced hirsutism, gingival hyperplasia, acne, alopecia, or cushingoid faci
11 asure the HQL impact of side effects such as gingival hyperplasia and facial hirsutism on physical ap
12 iated with Amelogenesis Imperfecta (AI) with gingival hyperplasia and nephrocalcinosis, while FAM20C
14 et, the molecular mechanisms of drug-induced gingival hyperplasia are unknown although it has been po
17 per presents an older patient with recurrent gingival hyperplasia due to plasminogen deficiency (hypo
21 indicating that amlodipine may also promote gingival hyperplasia; however, no data have been reporte
26 crodontism of primary teeth, and generalized gingival hyperplasia, whereas Sprengel deformity of scap
27 several undesirable side effects, including gingival hyperplasia, which occurs in up to 70% of patie
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