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Year : 2012  |  Volume : 3  |  Issue : 2  |  Page : 117-120

The plasma cell gingival enlargement: The diagnostic and esthetic concerns

1 Department of Periodontics and Oral Implantology, Sudha Rustagi College of Dental Sciences and Research, Faridabad, Haryana, India
2 Department of Oral Pathology, Sudha Rustagi College of Dental Sciences and Research, Faridabad, Haryana, India
3 Department Of Periodontics, National Dental College, Dera Bassi., Punjab, India

Date of Submission11-Apr-2012
Date of Acceptance29-Jun-2012
Date of Web Publication24-Jan-2013

Correspondence Address:
Sangeeta Dhir
Department Of Periodontics and Oral Implantology, Sudha Rustagi College of Dental Sciences and Research, Faridabad, Haryana - 121002
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0976-6944.106467

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Being a rare benign condition of the gingiva, PCG is characterized with erythematous and edematous gingivitis. The biologic phenomenon of the hypersensitive reaction appears to be chief etiology behind this occasionally presenting clinical entity. Plasma cell gingivitis has a close resemblance to discoid lupus, lichen planus, cicatricial pemphigoid or leukemia , and HIV gingivitis.It is known to present as a hypersensitive response to allergen, but sometimes it could present as a clinical entity with unknown etiology. The histological picture comprises of a dense infiltration of plasma cells separated with strands of collagen. Plasma cell gingivitis is a rare benign condition of the gingiva, which is marked with dense infiltration of the plasma cells separated with the strands of the collagen. The biologic phenomenon of the hypersensitive reaction appears to be chief etiology behind this occasionally presenting clinical entity. Plasma cell gingivitis has a close resemblance to discoid lupus, lichen planus, cicatricial pemphigoid or leukemia, and HIV gingivitis. We document herea case report of this clinical situation with an unusual gingival enlargement.

Keywords: Gingival enlargement plasma cell enlargement, hypersenstivity, plasma cell gingival enlargement, plasma cell gingivitis

How to cite this article:
Dhir S, Mehendiratta M, Malhotra R, Gupta G. The plasma cell gingival enlargement: The diagnostic and esthetic concerns. Indian J Oral Sci 2012;3:117-20

How to cite this URL:
Dhir S, Mehendiratta M, Malhotra R, Gupta G. The plasma cell gingival enlargement: The diagnostic and esthetic concerns. Indian J Oral Sci [serial online] 2012 [cited 2018 Jan 19];3:117-20. Available from: http://www.indjos.com/text.asp?2012/3/2/117/106467

  Introduction Top

Plasma cell gingivitis is primarily a hypersensitive response of the gingival with abundance of plasma cells in the connective tissues. The etiology is difficult to elicit; however specific known allergens have been found to be responsible, e.g., toothpaste, khat, food, chewing gum, and also of unknown origin. [1] The case presented here is a plasma cell gingivitis associated with unusual gingival enlargement in a 28-year-old patient.

  Case Report Top

Patient aged 28 years old reported to the Department of Periodontics, Sudha Rustagi College of Dental Sciences and Research, Faridabad, Haryana, with a chief complaint of unesthetic swelling of gums in upper and lower region of teeth since 3 months with burning sensation of the mouth on taking hot food. Oral examination revealed generalized severe gingival inflammation and enlargement covering up to the middle half of the clinical crown [Figure 1]. Erythema was pronounced in relation to the maxillary and mandibular anterior region. There was no loss of attachment. Generalized pseudo pockets ranged from 6mm to 9mm. Bleeding on slight manipulation. Macroscopically the gingiva appeared oedematous with loss of stippling. The medical, dental, and personal history of the patient was noncontributory. Investigative hematologic examination didn't reveal any significant finding. Minimal local deposits were found in the mouth. Phase 1 therapy, gingivectomy, to be followed by the histopathologic assessment of the erythmatous lesion, was planned. Phase 1 therapy did improve the tissue consistency moderately. Anti allergic drug cetzine (10 mg) (GlaxoSmithline) was prescribed to be taken orally thrice a day for 5 days Patient was advised to aviod spicy food. Combinedly the results were appreciable. Laser-assisted gingivectomy and gingivoplasty was performed [Figure 2] and [Figure 3]. The tissue specimen was sent for the histopathologic examination. The histopathologic examination revealed a hyperplastic, spongiotic epithelium with areas of thin long rete-ridges representing the classical psoriasiform pattern and pseudo-epitheliomatous hyperplasia. Leucocytic exocytosis and areas of neutrophillic microabcess were evident in the superficial layer without the presence of candidal hyphae being confirmed by periodic acid schiff (PAS) staining [Figure 3]. The lamina propria revealed extremely dense infiltration of chronic inflammatory cell infiltrate that was composed predominantly of plasma cells [Figure 4] and [Figure 5]. Few Russel bodies and numerous dilated vascular channels were consistently seen throughout the stroma. Based on the histologic examination a diagnosis for plasma cell gingivitis was made [Figure 6]. Postoperative results were satisfactory and there has not been any recurrence of the condition [Figure 7]. The patient is under follow-up care.
Figure 1: Preoperative

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Figure 2: Gingival enlargement pseudopocket

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Figure 3: Postopeative laser gingivectomy

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Figure 4: Spongiotic hyperplastic epithelium with underlying dense plasmacytic infiltrate and prominent dilated capillaries (H and E, x100)

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Figure 5: Spongiotic hyperplastic epithelium exhibiting neutrophilic microabcesses and exocytosis (H and E, x400)

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Figure 6: Dense plasmacytic infiltrate in stroma (H and E, x1000)

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Figure 7: Postoperative

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  Discussion Top

Allergic stomatitis results from the delayed hypersensitivity reaction that occurs when antigens of low molecular weight penetrate the skin or mucosa of susceptible individuals. These antigens combine with epithelial-derived proteins to form haptens that bind to langerhans cells in the epithelium. The langerhans cells migrate to the regional lymph node and present the antigen to T lymphocyte that become sensitized and undergo clonal expansion. After re-exposure to the antigen, sensitised individuals develop an inflammatory reaction confined to the site of contact. The incidence of the contact stomatitis is unknown but it is believed to be significantly less common than contact dermatitis owing to the attributed reasons: saliva quickly dilutes the potential antigens and physically washes them away and digests them before they can penetrate the oral mucosa, and oral mucosa being more vascular than skin doesn't allow the potential antigens to penetrate the mucosa and are rapidly removed before an allergic reaction can be established.

Contact stomatitis of oral origin may result from several reactions to cinnamon, [2] peppermint, flavoring agents in the food, candy and chewing gums, and oral hygiene products such as toothpaste, mouthwash, and dental floss. [3] Dental materials reported to cause contact stomatitis are mercury in amalgam, gold in crown, free monomer in the acrylic, and nickel in the orthodontic wire. [4],[5] Other sources of the contact stomatitis reported are the pyrophophates and zinc citrate, the important ingredients of the tartar control toothpaste. [6]

PCG is an uncommon condition marked with an intense and diffuse infiltration of the plasma cells into the subepithelial gingival tissue. [7] The prime etiology of this condition has not been ruled out; however it has been hypothesized that the immunologic reaction to some allergic antigen might be the possible causative agent. Mint in the toothpaste and chewing gum, [8] cinnamonaldehyde, [2],[3] strong spices (pepper,cardamom) /chillies, chewing of khat [9],[10] certain constituents of the herbal toothpastes have been documented as the reported allergens in the literature. [7] A historical perspective of this condition dates back to the year 1952 when Zoon referred the term "plasma-cell infiltrate." Kerr and his associates in the year 1971 revealed the most causative agent responsible for the allergic response--chewing gum. He observed that if the patients discontinued the use of the chewing gum the tissues returned to normal.

According to the etiology plasma cell gingivitis is categorised as lesions of unknown cause, lesions owing to some allergen, and lesions due to neoplastic origin. [11] Bleeding on the slightest manipulation is an invariable feature. [1],[11] There is usually no loss of attachment but loss of stippling. [1] The incidental clinical resemblance of the plasma cell gingivitis to the gingival changes as seen in leukemia lichen planus and cicatricial pemphigoid does require thorough serologic and hematologic testing. [12] PCG being a benign condition remits after detection and elimination of the etiologic agent. [13]

Plasma cell gingival enlargement with an idiopathic /unknown etiology is rare.To the authors knowledge only 3 cases have been documented till 2011. In this case the specific allergen could not be ruled from the history of the patient; however the symptomatic relief experienced by the patient by stopping spicy food and the fact that the antiallergic drug did improve the clinical picture of the case does pinpoint unknown cause. The highlight of this case is the exaggerated response of the gingiva in the form of enlargement associated with minimal etiologic factor (plaque and calculus). Case is being followed up. Plasma cell gingivitis, although a remote clinical entity, is of clinical significance. All efforts should be made for the management and meticulous follow up especially in cases with an unknown etiology. [14]

  References Top

1.Carranza FA, Hogan EL. Gingival enlargement. In: Fermin C, editor. Clinical Periodontology, 9 th ed. India: Saunders; 2003.p. 287-88.  Back to cited text no. 1
2.Lamey PJ, Lewis MA, Rees TD, Fowler C, Binnie WH, Forsyth A. Sensitivity reaction to the cinnamonaldehyde component of toothpaste. Br Dent J 1990;168:115-18.  Back to cited text no. 2
3.Miller RL, Gould AR, Bernstein ML. Cinnamon-induced stomatitis venenata, Clinical and characteristic histopathologic features. Oral Surg Oral Med Oral Pathol 1992;73:708-16.  Back to cited text no. 3
4.Pang BK, Freeman S. Oral lichenoid lesions caused by allergy to mercury in amalgam fillings. Contact Dermatitis 1995;33:423-27.  Back to cited text no. 4
5.Markussan JA. Contact allergies to nickel sulfate, gold sodium thiosulfate and palladium chloride in patients claiming side effects from dental alloy components. Contact dermatitis 1996;34:320-3.   Back to cited text no. 5
6.Kowitz G, Jacobson J. The effect of tartar control toothpaste on the oral soft tissue. Oral Surg Oral Med Oral Path Oral Radiol Endod 1992;73:690-95.   Back to cited text no. 6
7.DeRossi SS, Greenberg MS. Intraoral contact allergy-a literature review and case report. JADA 1998;129:1435-40.  Back to cited text no. 7
8.Kerr DA, McClatchey KD. Allergic gingivostomatitis due to gum chewing. J Periodontol 1971;42:709-12.  Back to cited text no. 8
9.Kalix P. Khat: A plant with amphetamine effects. J Subst Abuse Treat 1988;5:163-9.  Back to cited text no. 9
10.Marker P, Krogdhal A. Plasma cell gingivitis apparently related to the use of khat. Report of a case. BDJ 2002;192:311-3.  Back to cited text no. 10
11.Patanwala A, Fischer EW, Chappel LL. Plasma cell gingivitis affecting the gingiva, palatal mucosa and laryngeal cords. Perio 2006;3:123-8.  Back to cited text no. 11
12.Poswillo D. Plasmacytosis of the gingiva. Br J Oral Surg 1968;5:194-202.  Back to cited text no. 12
13.Macleod RI, Ellis JE. Plasma cell gingivitis related to the use of herbal toothpaste. Br Dent J 1989;166:375-76.  Back to cited text no. 13
14.Damm DD, Allen CM, Bouqout JE. Periodontal disease in oral and maxillofacial pathology in: 2nd ed. India: WB Saunders; An imprint of Elsevier;2002. p. 68-71.  Back to cited text no. 14


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]


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