This is caused by tissue edema and infective cellular infiltration caused by prolonged exposure to bacterial plaque, and is treated with conventional periodontal treatment, such as scaling and root planing.Gingivitis and gingival enlargement are often seen in mouth breathers, as a result of irritation brought on by surface dehydration, but the manner in which it is caused has not been demonstrated.The accumulation and retention of plaque is the chief cause of inflammatory gingival enlargement. Risk factors include poor oral hygiene, as well as physical irritation of the gingiva by improper restorative and orthodontic appliances. Drug-induced enlargement
This type of gingival enlargement is sometimes termed "drug induced gingival enlargement" or "drug influenced gingival overgrowth", abbreviated to "DIGO". Gingival enlargement may also be associated with the administration of three different classes of drugs, all producing a similar response: Gingival overgrowth is a common side effect of phenytoin, termed "Phenytoin-induced gingival overgrowth" (PIGO). anticonvulsants (such as phenytoin, phenobarbital, lamotrigine, vigabatrin, ethosuximide, topiramate and primidone NOT common for valproate)
calcium channel blockers (antihypertensives such as nifedipine, amlodipine, and verapamil). The dihydropyridine derivative isradipidine can replace nifedipine and does not induce gingival overgrowth. cyclosporine, an immunosuppressant.Of all cases of DIGO, about 50% are attributed to phenytoin, 30% to cyclosporins and the remaining 10-20% to calcium channel blockers. Drug-induced enlargement has been associated with a patients genetic predisposition, and its association with inflammation is debated.
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.