A clinical review of drug‐induced gingival overgrowths

Abstract

There is an increasing number of medications associated with gingival overgrowth. These medications are used to treat a number of common conditions in the Australian population and as such dentists can expect to manage a number of patients with medication-related gingival overgrowth. This review highlights the clinical features and management of the common overgrowths associated with anticonvulsants, immunosuppressants and the calcium channel blockers.

Management of Phenytoin Induced Gingival Overgrowth: A Case Report

“…Literature shows that there is a huge possibility which leads to the gingival changes such as multiple anti-epileptic therapies, plaque deposition, host genetic factors, and reduced serum folate levels [5]. The general agreement would be that, gingival hyperplasia is seen in patients under pheytoin is mainly the consequence of the increase in amount of connective tissue rather than a marked epithelial hyperplasia [6][7]. Literatures also suggest that major change in phenytoin gingival hyperplasia is due to the increase number of collagen but it still remains unclear if its caused by the increased number of fibroblast or elevated cellular activity [8][9][10][11].…”

“…TYPE 3 Combined enlargement. This is a combination of hyperplasia caused by phenytoin and inflammation by local irritation table 1 Drug substitution would be one of the most important steps in treating and preventing recurrence of gingival enlargement [6,[19][20]. Newer drugs such as lomatrigine, gabapentin, sulthiame, and topiramate can be opted as a drug substitute.…”

Connective Tissue Metabolism and Gingival Overgrowth

“…These medications include the anti-seizure drug phenytoin, the immune suppressor cyclosporin A, and certain anti-hypertensive dihydropyridine calcium-channel-blockers, most notably nifedipine. Clinical characteristics of different forms of gingival overgrowth have been previously reviewed (Hassell and Hefti, 1991;Marshall and Bartold, 1999;Seymour et al, 2000). There is now general agreement that gingival overgrowth lesions all contain fibrotic or expanded connective tissues with various levels of inflammation and an enlarged gingival epithelium.…”

Molecular and Clinical Aspects of Drug-induced Gingival Overgrowth

“…As already amply summarized by us and others, gingival overgrowth leads to compromised quality of life for patients, and can lead to indirect negative effects on systemic health (Hassell and Hefti 1991;Marshall and Bartold 1999;Seymour et al 2000;Trackman and Kantarci 2004;Wright et al 2005;Bharti and Bansal 2013). Present and future novel cellular mechanisms discovered in analyses of gingival overgrowth may have relevance to other oral diseases, most notably oral cancer, and neurofibromatosis-1, with the latter often accompanied by gingival overgrowth and tongue lesions which can progress to oral cancer (Cunha et al 2004;Jouhilahti et al 2012).…”

“…Non-surgical therapies to treat gingival overgrowth and stabilize the long-term outcomes are needed to alleviate suffering for those who are adversely affected. In addition to drug-induced gingival overgrowth, inherited and idiopathic forms of this condition, while rare, occur and have been reviewed previously (Hassell and Hefti 1991;Marshall and Bartold 1999;Seymour et al 2000;Trackman and Kantarci 2004;Bharti and Bansal 2013). Although progress in the clinical management of human gingival overgrowth has been made in relatively affluent societies, approaches of drug substitutions and careful dose adjustments are not universally practiced by physicians worldwide, and this contributes to the global public health impact of gingival overgrowth (Bharti and Bansal 2013).…”