Why Is Plasma Cell Gingivitis a Significant Clinicopathologic Entity?
Plasma cell gingivitis (PCG) is a benign condition of the gingival tissues that may be uncommon yet significant in occurrence. This condition, though benign, involves chronic and severe inflammatory patterns of gingival disease and is specifically characterized by dense infiltration of normal plasma cells that, in turn, get separated into multiple aggregates through collagenous strands or tissue. The importance of PCG disease lesions is that they not just cause severe gingival inflammation making the patient prone to oral discomfort or bleeding and pain, but also mimic many serious conditions such as HIV lesions of the oral mucous membrane, precancers, and oral tumors (leukemia). So the dentist should be very cautious in making differential diagnoses (given that the occurrence of PCG is relatively rare compared to other serious oral lesions or diseases).
Clinically, PCG manifests with lesions that present with diffuse redness and inflamed area on the gingival tissues. These edematous swellings observed in the gingival lesions may also have a sharp demarcation with the mucogingival border or edge.
What Is the Etiology of Plasma Cell Gingivitis?
The etiology of PCG remains elusive and unclear. However, research can hypothesize it because of the obvious presence of plasma cell inflammatory aggregates. It may most often be a tissue response of the gingiva in reaction to certain agents, i.e., in simple terms, it may be deemed an immunological reaction to specific allergens.
Commonly observed from dental literature and research, these allergens would range from ingredients that are used in common day-to-day use like toothpaste, chewing gums, certain allergenic foods, foods that contain herbs and strong spices like chili, pepper, clove, cardamom, or even mint. In the year 1971, Kerr et al. initially reported a case of PCG in a patient who suffered an allergic reaction to a flavoring agent used in chewing gum with the identified allergen or ingredient in the chewing gum as cinnamon. Since then, persistent dental research and cases occasionally reported in dental literature have supported that certain flavoring agents like cinnamaldehyde and cinnamon used in chewing gums or even dentifrices can prove potential stimulators or allergens for developing plasma cell gingivitis. Case reports also showcase that flavoring agent in both chewing gum and dentifrices are capable of producing inflammatory reactions either or on both attached and free gingival tissues. The inflammatory reaction is firstly characterized by intense erythematous changes post is the common chief complaint of the patient, bleeding from the mouth, i.e., via the gingival tissues.
What Is the Differential Diagnosis of Plasma Cell Gingivitis?
This is the most crucial step for treatment planning in plasma cell gingivitis cases. Similar clinical features that tend to resemble plasma cell gingivitis, like erythema, edematous gingival margins, demarcated lesion borders, bleeding, etc, are also found and need to be differentiated from these enlisted conditions:
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HIV (human immunodeficiency virus) infection’s oral lesions.
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Discoid lupus erythematosus.
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Desquamative gingivitis.
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Leukemia.
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Atrophic form of lichen planus.
Serologic and hematologic testing and tissue biopsy of the involved lesions for histopathologic examination and analysis will clearly help the oral pathologist gain a correct perspective on the nature of the lesion. Also, PCG lesions test negative for the Nikolsky sign and are characterized by a lack of cutaneous or skin-based lesions. Hence establishing the confirmative diagnosis is pivotal for treatment planning in this uncommon inflammatory condition that requires extensive treatment.
What Is the Management of Plasma Cell Gingivitis?
Plasma cell mucositis, commonly termed by dentists and it can be treated with medical and surgical approaches. The treatment modalities may not be of much value in relieving the clinical symptoms of the patient. This is because the fundamental agent or allergen that causes PCG needs to be detected, and it is a diagnostic challenge to find out the antigenic agent causing the immune inflammatory reaction in the gingiva. However, to improve the oral well-being and status of the patient, several treatment modalities have been tried and tested for this condition with an unclear success rate. These methods include:
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Corticosteroid therapy by topical corticosteroid application or intralesional injection of recommended corticosteroid by the maxillofacial surgeon.
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Systemic antibiotic therapies.
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Electrocoagulation.
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Liquid nitrogen therapy.
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Use of CO2 laser.
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Surgical excision of the affected tissue accompanied by radiation therapy if needed. This treatment is followed if none of the above modalities are effective in eliminating PCG.
The patient should also be regularly and repeatedly followed up in order to assess their personal oral hygiene maintenance and to identify the possible allergen for preventing a fresh recurrence of the PCG lesions. As the particular agent responsible for the immune allergic reaction may not be exactly identified, treatment protocols for these patients may be challenging in the long run, owing to repeated surgical excisions because of recurrent gingival enlargement. Hence in order to facilitate plaque control and maintain oral hygiene status, repeated surgical excision may be an alternative long-term surgical strategy in severe cases of PCG.
Conclusion:
To conclude, even though plasma cell gingivitis may be an uncommon and benign condition of the gingiva, occurring in response to a specific allergen, the identification and treatment strategies for the lesions are challenging for the maxillofacial surgeon. Also, as PCG mimics other oral lesions of serious nature like leukemia and myeloma, early diagnosis and timely oral management by the oral surgeon or dentist is of crucial importance. The oral surgeon should strive to detect and eliminate repeated exposure to the antigenic agent that would bring about the potential remission of plasma cell gingivitis.
