Some investigators assert that underlying inflammation is necessary for the development of drug-induced enlargement, while others purport that the existing enlargement induced by the drug effect compounds plaque retention, thus furthering the tissue response. Careful attention to oral hygiene may reduce the severity of gingival hyperplasia. In most cases, discontinuing the culprit drug resolves the hyperplasia. Enlargement associated with systemic factors
Many systemic diseases can develop oral manifestations that may include gingival enlargement, some that are related to conditions and others that are related to disease:
Conditioned enlargement
pregnancy
puberty
vitamin C deficiency
nonspecific, such as a pyogenic granuloma
Systemic disease causing enlargement
leukemia
granulolomatous diseases, such as granulomatosis with polyangiitis, sarcoidosis, or orofacial granulomatosis. neoplasm
benign neoplasms, such as fibromas, papillomas and giant cell granulomas
malignant neoplasms, such as a carcinoma or malignant melanoma
false gingival enlargements, such as when there is an underlying bony or dental tissue lesion

Mechanism
Drug Induced gingival overgrowth:

Fibrotic type:
Elevated CTGF (a.k.a. CCN2) which is a matricellular protein known to be reliable for fibrosis.TGF-β increases drives CTGF/CCN2 (current molecular mechanisms unknown), but supports TGF-β as a therapeutic target. CTGF is not down regulated in presence of inflammatory mediators (such as PGE2), unlike other tissues fibroblasts (such as kidney) which have their CTGF levels down regulated by the same PGE2. Inflammatory Type

Management
The first line management of gingival overgrowth is improved oral hygiene, ensuring that the irritative plaque is removed from around the necks of the teeth and gums.
A myxoid cyst is a cutaneous condition often characterized by nail plate depression and grooves. See also
Scleroderma
List of cutaneous conditions
List of radiographic findings associated with cutaneous conditions


== References ==