|Year : 2016 | Volume
| Issue : 4 | Page : 424-427
Gingival plasma cell granuloma: An occult lesion of rare origin
Susmitha Hosagadde Rathnakara, Mahesh Mysore Shivalingu, Srisha Basappa, Archana Patil
Department of Oral Medicine and Radiology, Farooqia Dental College and Hospital, Mysuru, Karnataka, India
|Date of Submission||14-Apr-2016|
|Date of Acceptance||21-Jan-2017|
|Date of Web Publication||21-Feb-2017|
Dr. Susmitha Hosagadde Rathnakara
Department of Oral Medicine and Radiology, Farooqia Dental College and Hospital, Mysuru - 570 021, Karnataka
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Plasma cell granuloma (PCG) is an exceedingly rare non-neoplastic lesion. The pathogenesis of the PCG remains unclear. It manifests as a localized, benign proliferation of polyclonal plasma cell population. It occurs primarily in the lungs but may also occur on other anatomical structures including the oral cavity, with gingiva being the rarest site. Here, we report the case of a 55-year-old female with two nodular growths seen on the left maxillary and mandibular posterior gingiva, which gave an impression clinically as pyogenic granulomas and histopathologically as nonspecific pathological entities. Advanced investigations such as immunohistochemistry was done, which ruled out other potential plasma cell neoplasms and confirmed the diagnosis of PCG.
Keywords: Immunohistochemistry, Kappa light chains, Lambda light chains, plasma cell granuloma, pyogenic granuloma
|How to cite this article:|
Rathnakara SH, Shivalingu MM, Basappa S, Patil A. Gingival plasma cell granuloma: An occult lesion of rare origin. J Indian Acad Oral Med Radiol 2016;28:424-7
|How to cite this URL:|
Rathnakara SH, Shivalingu MM, Basappa S, Patil A. Gingival plasma cell granuloma: An occult lesion of rare origin. J Indian Acad Oral Med Radiol [serial online] 2016 [cited 2019 Jul 16];28:424-7. Available from: http://www.jiaomr.in/text.asp?2016/28/4/424/200646
| Introduction|| |
Plasma cell granuloma (PCG) is an uncommon tumor of unknown etiopathogenesis. It manifests primarily in the lung and has been reported at anatomical sites such as the vagina, bladder and larynx including the head and neck region. In the head and neck region, it can be seen involving the orbit, paranasal sinuses, pterygomaxillary space, tonsils, ears, tongue, lips, oral mucosa and rarely the gingiva. Microscopically, it is characterized by vascular stroma and reactive inflammatory cells with predominance of plasma cell infiltrate resembling the initial stages of plasmacytoma, a soft tissue neoplasm of plasma cells. Radiologically few reported lesions have shown alveolar bone destruction with infiltrative margins giving an appearance of malignant tumor. Therefore, such lesions should be thoroughly evaluated to decide the exact nature of these lesions.
| Case Report|| |
A 55-year-old female patient visited the Department of Oral Medicine and Radiology with a complaint of mobile teeth associated with two swellings in the left upper and lower back teeth region since 5 months. Patient gave a history of noticing two small swellings in the left upper and lower posterior teeth region 5 months back, which was then associated with mobile teeth, following which she underwent extraction of the same. Swellings did not subside even after extraction followed by a course of antibiotics. Swellings gradually increased in size to attain the present size. Except for bleeding while brushing, no history of any other secondary changes was noted. Medical history revealed that the patient was hypertensive and had hypothyroidism, for which she was taking medication since 8 years.
On local examination of the maxillary and mandibular regions, on the left side, two separate nodular sessile growths, roughly measuring approximately 3 × 2 cm were present on the buccal aspect of 27, 28 and 37, 38. Mucosa over the growths appeared erythematous without any secondary changes [Figure 1]. On palpation, growths were firm in consistency, nontender, nonfluctuant and noncompressible. Associated teeth 27 and 37 were grade 2 mobile. Pathological mesial migration of 37 was noted. A provisional diagnosis of pyogenic granuloma was made for both the maxillary and mandibular lesions. Lesions such as fibrous epulis, peripheral giant cell granuloma and peripheral ossifying fibroma were considered in differential diagnosis. Routine investigations such as complete hemogram reported all values within the normal range. Intraoral periapical radiographs revealed 27 with vertical bone loss till apical one-third of its roots [Figure 2], and 37 having floating tooth appearance with irregular radiolucency surrounding the tooth [Figure 3].
|Figure 2: Intraoral periapical radiograph of 27 with vertical bone loss till apical one-third of its roots|
Click here to view
|Figure 3: Intraoral periapical radiograph of 37 having floating tooth appearance with irregular radiolucency surrounding the tooth|
Click here to view
Microscopic examination of incisional biopsy specimen revealed histopathological diagnosis of nonspecific inflammatory lesion. The lesions were surgically excised under local anesthesia along with extraction of 27, 37 and was sent for histopathological investigation. Hematoxylin and eosinophilic sections of both the lesions revealed stratified squamous epithelium and stroma showing inflammatory infiltrate with abundant plasma cell component along with areas of fibrosis [Figure 4]. History and clinical features were correlated with the histopathological findings of predominance of plasma cells in the stroma of the lesions, which suggested a diagnosis of PCG of gingiva. Advanced investigation with immunohistochemistry was done for Kappa and Lambda light chains to confirm the clonality of plasma cells and to rule out any plasma cell neoplasm. A strong positivity for both Kappa and Lambda chains were seen, which suggested the polyclonal plasma cell population, revealing its reactive and inflammatory nature [Figure 5]. Thus, a final diagnosis of PCG of gingiva was confirmed for both the maxillary and mandibular lesions in our case.
|Figure 4: Tissue sections (maxillary and mandibular lesions) stained with hematoxylin and eosin viewed at 40× magnification showing stroma with inflammatory infiltrate of abundant plasma cell component|
Click here to view
|Figure 5: Immunohistochemistry (maxillary and mandibular lesions) showing positivity for Kappa and Lambda light chains|
Click here to view
| Discussion|| |
PCG is an extremely rare, benign reactive lesion of inflammatory origin. The exact incidence, biologic behavior, and causative factors of this lesion are unclear, and little is known about the prognosis. Histologically, it consists of a proliferation of inflammatory cells, with a predominance of plasma cells in a fibrovascular background. Rarely seen in the oral cavity, the lesions are usually single, and are primarily seen on the periodontal tissue, mainly the gingiva, followed by tongue, lips, buccal mucosa and palate. The World Health Organization describes it as an intermediate (rarely metastasizing) fibroblastic/myofibroblastic tumor composed of myofibroblastic spindle cells accompanied by inflammatory infiltrate of plasma cells, lymphocytes, and eosinophils. Other names used in literature are inflammatory pseudotumor, histiocytoma, xanthomatous granuloma, inflammatory myofibroblastic tumor, and spindle cell pseudotumor. Plasma cells are terminally differentiated B lymphocytes which are typically found in the red pulp of the spleen, medulla of the lymph nodes, tonsils, lamina propria of the entire gastrointestinal tract, mucosa of the nose and upper airway, and sites of inflammation.
The exact etiology of PCG is not known. The histologic diversity has led to conflicting opinions regarding the inflammatory or neoplastic nature of this lesion, with majority of reports agreeing with the postinflammatory reactive process. The plasma cells are polyclonal favouring inflammatory nature. However, spindle cells of some lesions have been shown to possess a persistent abnormality involving chromosome 2p23 an ALK gene locus, which is consistent with the neoplastic nature of this lesion. The finding of human herpesvirus-8 DNA sequences and overexpression of human interleukin 6 and cyclin D1 have also been reported in seven cases. It is often singular and is associated with some chronic antigenic exposure. This could be because of periodontitis, periradicular inflammation or foreign bodies. The large number of plasma cells may represent an autoimmune reaction or an alteration of blood flow imposing congestive vasodialation (angioplasmacellular hyperplasia). It is also thought to be a result of inflammation following minor trauma or surgery or to be associated with malignancy.
In 1968, Bhaskar, Levin and Firch first reported cases of gingival PCG, and in 1973, Bahadori and Liebow described PCG as an uncommon, non-neoplastic lesion. Since then very few case reports have been documented. PCG of gingiva can occur at any age, predominantly observed at 4th and 5th decade with slight female predilection. Exact incidence is unclear. In 2011, Kim and Lee described 14 cases of PCG out of 59 chronic inflammatory gingival lesions examined and divided PCG into three histological types, namely, plasma cell predominant type (PPT), mixed inflammatory cell type (MICT) and sclerosed fibrosis type (SFT). The results of immunohistochemical studies on these cases suggest a variable gene expression for cell mediated immunity and stromal tissue degeneration, undergoing sclerotic fiborsis with a persistent inflammatory reaction. The stroma is collagenous or myxoid.
The differential diagnosis of plasma cell predominant conditions affecting gingiva that could be considered are plasmacytoma and plasma cell gingivitis. Plasmacytoma comprises diffuse sheets of neoplastic, variably differentiated and monoclonal plasma cells. Mitotic activity and amyloid deposition may be present and inflammatory cells are very sparse. The present case showed predominance of plasma cell infiltrate in the connective tissue stroma. Immunohistochemistry showed polyclonal plasma cells. The other polyclonal lesions of gingiva include plasma cell gingivitis, which is usually not a localized nodular lesion but presents as generalized edematous and erythematous elevations.
Radiographically, PCG may or may not be associated with alveolar bone destruction. A case report by Telang et al. has radiographically shown advanced crestal bone loss with ill-defined radiolucency surrounding the apices of the teeth. Routine laboratory findings are normal. Immunohistochemistry determines the clonality of the plasma cells in the lesion, wherein in a reactive lesion, the Kappa and Lambda light chain ratio is 2:1, and in the case of malignancy the ratio may be greater than 10:1. It is important to differentiate PCG from extramedullary plasmacytoma considering the poor prognosis of this neoplasm. Management of PCG involves simple excision, as it is benign, and eliminating the underlying causative agent, whereas neoplasms may require surgical excision followed by chemotherapy and/or radiotherapy.,,, Prognosis of PCG is good as there is no evidence of recurrence in any of the reported cases. In our case, simple excision was found to be curative followed by an uneventful healing period with no sign of recurrence [Figure 6].
|Figure 6: Postoperative images of maxillary and mandibular regions after 2 months of follow up|
Click here to view
| Conclusion|| |
Gingival PCG is an extremely rare entity with clinical features similar to other chronic inflammatory or reactive lesions of the oral cavity. Histopathologically, it mimics soft tissue neoplasms of plasma cells, necessitating further investigations such as immunohistochemistry to rule out any malignancy. This case report reinforces the existence of PCG on gingiva and emphasizes the importance of proper evaluation of any lesions with appropriate diagnostic techniques to prevent unnecessary extensive surgical procedures.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Telang A, Telang LA. Oral plasma cell granuloma: An enigmatic lesion. Int J Oral Maxillofac Pathol 2013;4:64-7.
Pandav AB, Gosavi AV, Lanjewar DN, Jagadale RV. Gingival plasma cell granuloma. Dent Res J 2012;9:816-20.
Jawanda MK, Narula R, Nirola A, Gupta S, Gupta P. Oral plasma cell granuloma. J Int Clin Dent Res Org 2014;6:55-8.
Jeyaraj P, Naresh N, Malik A, Sahoo NK, Dutta V. A rare case of gingival plasma cell granuloma of the gingiva masquerading as a gingival epulis. Int J Dis Dis 2013;1:16-9.
Bhaskar SN, Levin MP, Frisch J. Plasma cell granuloma of periodontal tissues. Report of 45 cases. Periodontics 1968;6:272-6.
Phadnaik MB, Attar N. Gingival plasma cell granuloma. Indian J Dent Res 2010;21:460-2.
Bansal N, Sheikh S, Bansal R, Sabharwal R, Kumar M, Goel A. Plasma cell granuloma of gingiva- A rare case report. Int J Sci Study 2013;1:155-8.
Manohar B, Bhuvaneshwari S. Plasma cell granuloma of gingiva. J Indian Soc Periodontol 2011;15:64-6.
Imran F, Rajan S, Vijay G. A case of plasma cell granuloma of unknown cause. J Orofac Res 2012;2:235-7.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]