International Journal of Clinical Case Reports 2017, Vol.7, No.5, 19-22
22
pathologic changes seen (Newman et al., 2006). The most common type of gingival enlargement seen is plaque
induced inflammatory gingival enlargement (Agrawal et al., 2011). This is seen as a result of cellular infiltration
and edema due to continuous insult caused by the bacterial plaque and is treated with conventional scaling and
root planning procedures (Buddiga et al., 2012). The regions wherein there is fibrous component which does not
respond to the conventional scaling and root planing are treated with surgical methods including gingivectomy or,
by modified Widman flap (Jhadhav et al., 2013). The bulging tissue forms pseudo pockets which are not self
cleansable and instead allow accumulation of food debris and microorganisms. A foul breath results due to
degradation of food debris. Along with the local factors, systemic factors may contribute to the severity of the
disease process and compromise the outcome of the therapeutic procedure done (Hassell and Jacoway, 1980). In
the present case report, inflammatory enlargement was present in relation to upper and lower anterior and upper
left posterior regions of jaws compromising esthetics. After non-surgical therapeutic procedure, upper anterior and
left posterior regions showed resolution of the inflammation whereas lower anterior region showed less resolution
as the fibrotic component was eminent while both upper and lower teeth showed presence of pockets which was,
then, corrected by the surgical therapy.
3 Conclusions
Gingival enlargement is largely diffuse in nature which can interfere in speech and mastication. Local factors such
as plaque and calculus are known to be the possible causatives for gingival enlargement. In the present case report,
increase in the size of gingiva resulted in unesthetic appearance; hence, non surgical therapy along with surgical
therapy was planned which resulted in resolution.
References
Agrawal N., Agrawal K., and Mhaske S., 2011, An uncommon presentation of an inflammatory gingival enlargement responding to non-surgical periodontal
therapy, Int J Dent Hyg, 9: 303-307
PMid:21356030
Buddiga V., Ramagoni N.K., and Mahantesh H., 2012, Gingival enlargement: A case series, Ann Essence Dent, 1: 73-76
Blackwell C.C., Weir D.M., James V.S., and Cartwright K.A.V., 1989, The Stonehouse study: Secretor status and carriage of Neisseria species, Epidemiol Infect,
120: 1-10
Effiom O.A., Adeyemo W.L., and Soyele O.O., 2011, Focal reactive lesions of the gingival: An analysis of 314 cases at tertiary health institution in Nigeria,
Niger Med J, 52: 35-40
Hassell T.M., 1980, Clinical and Scientific Approaches to Gingival Enlargement (II), Perio Oral Hyg, 11: 51-59
Hassell T.M., and Jacoway J.R., 1980, Clinical and Scientific Approaches to Gingival Enlargement (I), Perio Oral Hyg, 10: 1-5
Jhadhav T., Bhat K.M., Bhat G.S., and Varghese J.M., 2013, Chronic Inflammatory Gingival Enlargement Associated with Orthodontic Therapy: A Case Report,
J Dent Hyg, 87: 19-23
Newman M.G., Takei H., Klokkevold P.R., and Carranza F.A., 2011, Carranza's clinical periodontology, Elsevier health sciences,
10
th
ed. WB Saunders,
373-387
Seymour R.A., 2006, Effects of medications on the periodontal tissues in health and disease, Periodontol, 40: 120-129
PMid:16398689
Trackman P., and Kantarci A., 2004, Connective tissue metabolism and gingival overgrowth, Crit Rev Oral Bio Med, 15: 165-175
Tiwana P.S., Kok I.J., Stoker D.S., and Cooper L.F., 2005, Facial distortion secondary to idiopathic gingival hyperplasia: Surgical management and oral
reconstruction with endosseous implants, Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 100: 153-157
PMid:16037772
Wright H.J., Chapple L.C., and Ptair C., 2004, Cervicular fluid level of TGFB1 in drug induced overgrowth, Arch Oral Biol, 49: 421-425
PMid:15041490
