Effect of Intraepidermic Injection of Vitamin C on Collagen Production Compared to Fibrotic Hereditary Gingival Fibromatosis: Histopathological Study

Oral fibromatosis is a benign non-relevant condition that could be an idiopathic solitary manifestation, part of a syndrome or a manifestation associated with systemic disease as leukemia, epilepsy, etc. (Anegundi et al., 2006 and Hakkinen & Csiszar, 2007). It may be also associated with other minor manifestations as hypertrichosis (Pavone, 2015 and Sabina-Pena-Borges, 2015), anemia, gastro-intestinal disturbance and/ or hormonal disturbance. Up till now, the idiopathic form is a rare condition with no definite hypothesis that could explain its mechanism.

Clinically, the disease usually develop as fibrotic non-painful, pinkish, non-hemorrhagic lesions which can either relate to erupted teeth (deciduous or permanent) or edentulous areas (retromolar region, maxillary tuberosity). The lesions primarily erupt as nodular separate islands related to the interproximal papillae then gradually coalesce (Anegundi et al., 2006; Singhal, 2013 and Gawron et al., 2016).

By the development of such lesions, bad esthetics, speech problems, mastication problems, carious lesions, plaque accumulation are the main complaints of the patients suffer from. Bone loss as well as periodontitis may develop later on as a squeal of plaque accumulation and improper cleaning (Ramer et al., 1996 and Anegundi et al., 2006). The peak of enlargement usually accompanies the beginning of mixed dentition (Anegundi et al., 2006; Singhal, 2013 and Gawron et al., 2016).

According to literature, the genetic susceptibility showed the most reliable explanation to fibromatosis development. It may be transmitted as an autosomal dominant or recessive trait. Local factors also play an important role in disease exacerbation such as plaque, calculus, chemical agents, trauma, restorations, orthodontic appliances, fixed restorations (Anegundi et al., 2006).

Histologically, there is great debate if the enlargement's origin is more relevant to epidermis layer, dermis layer or both. In the epidermal theory, the epithelial layer is the initiating layer due to the epithelial mesenchyme transitions and the presence of keratinocyte growth factor (Boukamp et al., 1990) while in the dermal theory, the overproduction of the dense, fibrous and avascular extracellular matrix with differently oriented collagen bundles, marked reduction in collagenase formation are the initiating factors (Vardar et al., 2005; El-Firt, 2011; Pego et al., 2015). The name fibromatosis is related to the dermal hypothesis due to the over production of fibrous tissues. Finally, the coexistence of epithelial and connective tissue hyperplasia regards to fibroblasts and keratinocytes hyperactivity which supports the third theory (Boukamp et al., 1990).