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The confined clinical presentation, along with the heavy plasma cells intermixed with minimal collagen in histology, eliminates Drug Induced Gingival enlargement (in such cases, there would be an increase in dense collagen bundles along with fibroblasts)

Figure 3.1. Budding forms of fungi. (highlighted by arrow)

Immunostaining was ordered for further investigation. Results obtained highlighted plasma cells (CD38 positive) and no restriction of Kappa and Lambda light chains.

Figure 4.1. CD38 Positive plasma cells.

Figure 5.1. A) Lambda light chain IHC positive. B) Kappa IHC positive.

Discussion

The majority of PCGs occur in the respiratory system. However, various unusual locations were reported, like the skin and CNS. As mentioned previously, only a few cases have been reported in the gingiva [8]. The exact cause remains a conflict; nevertheless, the hypothesis that suggests that a non-specific inflammation to an unknown antigen stimulates immunity and the proliferation of plasma cells is the most accepted explanation [1]. The inflammatory process can be a consequence of anything from minor trauma to malignancy [6].

Clinically, the lesion appears as a smooth, painless mass. As the lesion grows, it becomes larger and, therefore, ulcerated. At that time, the patient may complain of pain [7]. Herein, the lesion was only 1cm, and the patient reported no pain. PCGs do not have a unique clinical presentation. Thus, they can be easily misdiagnosed at first, particularly in patients with complex medical histories. A paper that reported a case of PCG in a hypertensive patient on Amlodipine had initially favored the diagnosis of Drug-Induced Gingival Overgrowth [5]. That was certainly in the top differentials in our patient who was on Nifedipine and immunosuppressors. Tacrolimus is another drug that is popular for its effect on the gingiva. A study reported overgrowth in patients who have been taking it for as little as three months from transplant [9]. The patient in this paper had received his transplant five years ago. The impact of this drug cannot be ruled out.

In isolated advanced cases, bone destruction can be evident radiographically as an ill-defined radiolucency [13]. The role of histologic examination of these lesions is of great importance to exclude drug-induced lesions as well as neoplasms like multiple myeloma and plasmacytoma, especially in patients around their 60s [11]. Our patient is a 57-year-old, which puts him under the light.

Microscopically, plasma cells in sheets and aggregates are seen. They have an eccentric nucleus with a basophilic cytoplasm. These cells are arranged along with fibroblasts, histocytes, or other types of mesenchymal cells [2]. Several microorganisms have been associated with PCGs; these are mycobacteria, Epstein–Barr virus, actinomycetes, Nocardia, and mycoplasma [7]. Interestingly, in our case, budding yeast has been observed.

Management with surgical resection of the lesion is the treatment of choice with no recurrences in follow-up [14]. Along with the removal of the underlying cause if identified. The line of treatment with PCG is simple as opposed to plasmacytoma, which can require chemo or radiotherapy [13]. With our patient, excision of the nodule was found ideal.