Puberty Induced Gingival Enlargement: A Case Report

Headnote

Abstract

Systemic factors such as puberty menstrual cycle, pregnancy and diabetes may exacerbate the gingival inflammatory response to plaque. This altered response appears to result from the effects of systemic conditions on the host's cellular and immunologic functions. Gingival tissues and the subgingival microflora respond with a variety of changes to the increasing hormone level at the onset of puberty. Gingival enlargement in puberty is characterized by a nodular hyperplastic reaction of gingiva with increased gingival inflammation, without accompanying an increase in plaque levels. Increased prevalence of certain bacterial species such as Prevotella intermedia and Capnocytophaga species have been reported which are believed to be responsible for the increased bleeding tendency noted in puberty. A case of puberty induced gingival enlargement in a 15 year old female patient is presented here.

Keywords: Puberty, Oral manifestations, Gingival hyperplasia.

Introduction

Gingival hyperplasia is an atypical increase in the number of healthy cells in normal arrangement in a tissue. Gingival hyperplasia can be the result of unusual tissue response to the inflammation caused by local irritants, such as plaque and calculus; systemic disturbances, such as hormonal changes; or medications specifically cyclosporine, nifedipine and phenytoin.

The homeostasis of the periodontium involves complex multifactorial relationships, in which the endocrine system plays an important role.1 Hormones are specific regulatory molecules that modulate function, reproduction, growth and development and the maintenance of internal environments as well as energy production, utilization and storage.1 As well as being the regulators of reproductive functions, sex steroid hormones have potent effects on the nervous and cardiovascular system, on major determinants of the development and integrity of the skeleton and oral cavity including periodontal tissues.2Under the broad category of dental plaque induced gingival diseases that are modified by systemic factors, those associated with the endocrine system are classified as puberty, menstrual cycle and pregnancy associated gingivitis.3 Researchers have shown that changes in periodontal conditions may be associated with variations in sex hormones.4 Enlargement of the gingiva can sometimes occur during puberty. It occurs in both male and female adolescents and appears in areas of plaque accumulation. The size of the gingival enlargement greatly exceeds that usually seen in association with comparable local factors. It is marginal and interdental and is characterized by prominent bulbous interproximal papilla. Often, only the facial gingiva are involved and the lingual surfaces are relatively unaltered.

Case report

A female patient aged 15 years was referred to the Department of Periodontology and Oral Implantology I.TS-CDSR with a chief complaint of swollen gums and spontaneous bleeding from the anterior maxillary and mandibular region since one year. Patient was apparently well two years back when she started complaining of the gingival swelling, which started as an enlargement in the interdental region and gradually extended to involve the entire maxillary and mandibular anterior region. The patient also presented with a history of reduced brushing frequency due to the associated bleeding and discomfort. The medical history was non-contributory and there was no history of drug intake reported. The personal history revealed that she had entered her menarche one year back.

Intraoral examination revealed poor oral hygiene. A diffuse gingival enlargement involving the marginal, interdental and attached gingiva was observed. Gingival enlargement, nodular in appearance was confined to the labial aspect of the anterior segment, both maxillary and mandibular region. It appeared reddish pink in colour with melanin pigmentation (Figure 1). Bleeding on probing occurred with the slightest provocation. Radiographically no bone loss was evident. Blood counts were within normal range, althoughshewasfoundtobesufferingfrommildanaemia.

Oral prophylaxis including thorough removal of supra-gingival and subgingival plaque and calculus was performed. Instructions regarding maintenance of oral hygiene were given. After 15 days there was a gradual reduction in the size of the enlargement, with a definitive improvement in the gingival status. However due to the persistence of gingival overgrowth, surgical intervention including external bevel gingivectomy was performed (Figure 2,3,4) for both the maxillary and mandibular anterior segments and the excised tissue was sent for histopathological examination (Figure 5). The gingival tissues healed uneventfully within a month (Figure 6).

Bleaching of both the maxillary and the mandibular arches was also done to reduce the flourotic stains. 35% hydrogen peroxide (Pola office Patient kit, SDI limited, Australia) was used as a bleaching agent and applied to the tooth surfaces for 24 minutes (3 cycles of 8 minutes each) (Figure 7). The results obtained were esthetically pleasing. The histopathology revealed pseudoepithelomatous hyperplastic epithelium with prominence of thin walled blood vessels in sinusoidal pattern and pooling of red blood cells (RBC's) within the vascular lumen. Vasculitic changes were evident as presence of chronic inflammatory cells around the blood vessels. In the central portion collagen fibres were irregularly arranged, densely fibrous in nature whereas at the periphery they were hyalinized (FigureS).

Based on the age of onset, clinical findings and histopatho-logical examination, a diagnosis of puberty induced gingival enlargement was made.

Discussion

Puberty marks the initiation of changes from maturation into adulthood.5 It is associated with a major increase in the secretions of the sex steroid hormones, testosterone in males and estradiol in females. Several cross-sectional and longitudinal studies have demonstrated an increase in gingival inflammation without accompanying an increase in plaque levels during puberty. Increased gingival inflammation was positively correlated with an increase in serum estradiol and progesterone and was not accompanied by a significantchange in the mean plaque index.1

Gingival tissues and the subgingival microflora respond with a variety of changes to the increasing hormone level at the onset of puberty. Microbial changes have been reported during puberty and can be attributed to changes in the microenvironment seen in the gingival tissue response to the sex hormones, as well as the ability of some species of bacteria to capitalize on the higher concentration of hormones present.6 Clinically, during puberty there may be a nodular hyperplastic reaction of the gingiva in areas where food debris, materia alba, plaque and calculus are deposited. The inflamed tissues are deep red and may be lobulated, with ballooning distortion of the interdental papillae. Bleeding may occur when patients masticate or brush their teeth. Histologically, the appearance is consistent with inflammatory hyperplasia.

Gingival enlargement during puberty has all the clinical features associated with chronic inflammatory gingival disease. Itisthe degree of enlargement and the tendency to develop massive recurrence in the presence of relatively scant plaque deposits that distinguish pubertal gingival enlargement from uncomplicated chronic inflammatory gingival enlargement.

At puberty, the production of sex hormones (estrogen and progesterone) increases to a level that remains relatively constant throughout the normal female reproductive phase. Studies have shown that increased sex hormone levels correlate with an increased prevalence of gingivitis.7 Gingival tissues and the subgingival microflora respond with a variety of changes to the increasing hormone level at the onset of puberty. Microbial changes reported during puberty can be attributed to changes in the microenvi-ronment seen in the gingival tissue response to the sex hormones, as well as the tendency of specific bacteria to proliferate due to the higher concentration of hormones present.6 This is seen with Prevotella intermedia (P. intermedia), a gram-negative anaerobe that can substitute estrogen and progesterone for vitamin K, an essential growth factor.8 In addition, Capnocytophaga species. another gram-negative bacterimnf increases in incidence as well as in proportion. Both organisms are believed responsible for the increased bleeding tendency noted in puberty. A longitudinal studyof 127 children 11 to 17 years of age showed ahigh initial prevalence of gingival enlargement that tended to decline with age.9 When the mean number of inflamed gingival sites per child was determined and correlated with the time at which the maximum number of inflamed sites was observed and with the oral hygiene index at that time, a pubertal peak in gingival inflammation unrelated to oral hygiene factors clearly occurred. Gingival enlargement in puberty is treated by performing scaling and curettage, removing all sources of irritation and controlling plaque. Surgical removal may be required in severe cases.

Conclusion

It is clear that endogenous sex steroid hormones play significant roles in modulating the periodontal tissue responses and may alter periodontal tissue responses to microbial plaque and thus directly may contribute to periodontal disease. They can influence the periodontium at different life times such as puberty, menstruation, pregnancy, menopause and postmenopause. Thus a better understanding of the periodontal changes to varying hormonal levels throughout life can help the dental practitioner in the diagnosis and treatment.

References

References

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