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Plasma cell gingivitis
Plasma cell gingivitis
Plasma cell gingivitis
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Plasma cell gingivitis
Plasma cell gingivitis in an adult (histologically verified).

Plasma cell gingivitis[1][2] is a rare condition,[3] appearing as generalized erythema (redness) and edema (swelling) of the attached gingiva, occasionally accompanied by cheilitis (lip swelling) or glossitis (tongue swelling).[4] It is called plasma cell gingivitis where the gingiva (gums) are involved,[5] plasma cell cheilitis,[5] where the lips are involved, and other terms such as plasma cell orifacial mucositis,[5] or plasma cell gingivostomatitis where several sites in the mouth are involved. On the lips, the condition appears as sharply outlined, infiltrated, dark red plaque with a lacquer-like glazing of the surface of the involved oral area.[5]

Signs and symptoms

[edit]
Plasma cell gingivitis in 7-year-old child. Histologically verified.
Plasma cell gingivitis in a 10-year-old child. Histologically verified.

Plasma cell gingivitis appears as mild gingival enlargement and may extend from the free marginal gingiva on to the attached gingiva.[6] Sometimes it is blended with a marginal, plaque induced gingivitis, or it does not involve the free marginal gingiva. It may also be found as a solitude red area within the attached gingiva (pictures). In some cases the healing of a plaque-induced gingivitis or a periodontitis resolves a plasma cell gingivitis situated a few mm from the earlier plaque-infected marginal gingiva. In case of one or few solitary areas of plasma cell gingivitis, no symptoms are reported from the patient. Most often solitary entities are therefore found by the dentist.[2]

The gums are red, friable, or sometimes granular, and sometimes bleed easily if traumatised.[6] The normal stippling is lost.[7] There is not usually any loss of periodontal attachment.[6] In a few cases a sore mouth can develop, and if so pain is sometimes made worse by toothpastes, or hot or spicy food.[7] The lesions can extend to involve the palate.[7]

Plasma cell cheilitis appears as well defined, infiltrated, dark red plaque with a superficial lacquer-like glazing.[5] Plasma cell cheilitis usually involves the lower lip.[3] The lips appear dry, atrophic and fissured.[7] Angular cheilitis is sometimes present.[7]

Where the condition involves the tongue, there is an erythematous enlargement with furrows, crenation and loss of the normal dorsal tongue coating.[7]

Causes

[edit]

Plasma cell gingivitis and plasma cell cheilitis are thought to be hypersensitivity reactions to some antigen.[3][6] Possible sources of antigens include ingredients in toothpastes, chewing gum, mints, pepper, or foods.[7][6] Specifically, cinnamonaldehyde and cinnamon flavoring are often to blame.[3] However, the exact cause in most is unknown.[3]

Diagnosis

[edit]
Plasma cells in Plasma cell gingivitis. Light microscopy X450.

Histologically plasma cell gingivitis shows mainly plasma cells.[2] The differential diagnosis is with acute leukemia and multiple myeloma.[4] Hence, blood tests are often involved in ruling out other conditions.[3] A biopsy is usually taken, and allergy testing may also be used. The histopathologic appearance is characterized by diffuse, sub-epithelial plasma cell inflammatory infiltration into the connective tissue.[3] The epithelium shows spongiosis.[6] Some consider that plasmoacanthoma (solitary plasma cell tumor) is part of the same spectrum of disease as plasma cell cheilitis.[5]

Classification

[edit]

Depending upon the site of involvement, this condition could be considered a type of gingivitis (or gingival enlargement); a type of cheilitis; glossitis; or stomatitis. Sometimes the lips, the gums and the tongue can simultaneously be involved, and some authors have described this triad as a syndrome ("plasma-cell gingivostomatitis").[3] The mucous membranes of the genitals can also be involved by a similar condition, termed "plasma cell balanitis" [2] or "plasma cell vulvitis".[8]

Other synonyms for this condition not previously mentioned include atypical gingivitis, allergic gingivitis, plasmacytosis of the gingiva, idiopathic gingivostomatitis, and atypical gingivostomatitis.[3][7] Some of these terms are largely historical.

Plasma cell gingivitis has been subclassified into 3 types based upon the cause; namely, allergic, neoplastic and of unknown cause.[3]

Treatment

[edit]

Preventing exposure to the causative antigen leads to resolution of the condition.[6] Tacrolimus or clobetasol propionate have also been used to treat plasma cell cheilitis.[5]

Epidemiology

[edit]

Plasma cell gingivitis is rare, and plasma cell cheilitis is very rare.[3] Most people with plasma cell cheilitis have been elderly.[3]

History

[edit]

Plasma cell gingivitis was first described in the late 1960-early 1970s. A wave of cases occurred during this period, thought to be caused by allergic reactions to a component in chewing gum. Since, the number of cases has decreased, but they are still occasionally reported.[7]

See also

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References

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[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Plasma cell gingivitis

View on Grokipedia
from Grokipedia
Plasma cell gingivitis (PCG) is a rare, benign, non-plaque-induced inflammatory condition of the gingiva characterized by dense polyclonal infiltration in the subepithelial . It typically presents as diffuse, erythematous, and edematous , often affecting the anterior maxillary and mandibular regions and extending to the mucogingival junction, with symptoms including spontaneous bleeding and discomfort. The condition is most commonly linked to reactions to allergens such as , flavoring agents in toothpastes or gums, and products, though idiopathic cases also occur. Clinically, PCG manifests as bright red, velvety gingival lesions that may involve swelling and loss of gingival , predominantly in females aged 9–64 years based on reviewed cases. Histopathologically, it features acanthosis, , and a predominant infiltrate with eccentrically placed nuclei, confirmed by showing positive CD38 and CD138 markers without light chain restriction to differentiate it from malignancies like or . Diagnosis requires a comprehensive approach, including detailed , clinical examination, laboratory tests to rule out systemic diseases (e.g., , ), and to exclude mimics such as periodontitis, , or . Treatment focuses on identifying and eliminating potential allergens, followed by non-surgical periodontal therapy like , topical corticosteroids (e.g., or ), and supportive measures such as antihistamines. In refractory cases, surgical excision or emerging adjuncts like photobiomodulation may achieve remission, with low recurrence rates upon allergen avoidance and maintenance of , though long-term follow-up is recommended due to its potential for persistence. It may be associated with plasma cell .

Background

Definition

Plasma cell (PCG) is a rare, benign, non-plaque-induced inflammatory condition of the gingiva characterized by dense subepithelial infiltration of polyclonal s without neoplastic features. It represents an idiopathic proliferative disorder confined primarily to the gingival tissues, distinguishing it from systemic . Synonyms for the condition include atypical , allergic , plasma cell gingivosis, idiopathic gingivostomatitis, and plasma cell gingivostomatitis. Key clinical and histological characteristics of PCG encompass gingival hyperplasia, , and , often presenting as diffuse enlargement of the free and attached gingiva. Histologically, the condition features aggregates of s within the subepithelial , separated by strands of fibrous tissue, with no disruption of the overlying epithelium's normal architecture. These collections are polyclonal, lacking cytological or monoclonal light chain restriction, which helps differentiate PCG from periodontal diseases like periodontitis—where attachment loss and plaque accumulation are prominent—and from malignancies such as plasma cell neoplasms or . When accurately diagnosed, PCG carries a benign , with no typical progression to attachment loss or reported in the . The condition remains localized to the gingiva and does not indicate an increased risk for systemic disorders like or .

Historical Development

Plasma cell gingivitis was first described in the late as a distinct clinical entity characterized by gingival with prominent infiltration. In 1969, Owings reported four cases of atypical gingivostomatitis, noting sharply demarcated gingival and alongside histopathological evidence of dense accumulations, initially raising concerns for a neoplastic process. Key early reports from to 1973 increasingly linked the condition to reactions, particularly to flavorings in consumer products. For instance, Kerr et al. in 1971 detailed cases of idiopathic gingivostomatitis involving , , and , attributing the lesions to allergic responses to in cinnamon-flavored chewing gums, with resolution following avoidance. Similar associations were noted in subsequent publications during this period, establishing flavoring agents like as common triggers in what was then termed a wave of related cases. Following this initial surge, reports of plasma cell gingivitis declined in the late 1970s, likely attributable to modifications in product formulations that reduced exposure to implicated allergens such as certain gum flavorings. Cases persisted sporadically thereafter, with literature emphasizing broader hypersensitivity etiologies including toothpastes and spices, rather than solely cinnamon derivatives. A resurgence in documented instances appeared in the late 20th and early 21st centuries, reflecting improved diagnostic awareness and diverse allergen sources. Recent studies, such as a 2023 retrospective analysis, have noted a potential increase in cases post-COVID-19 pandemic, with diagnoses rising threefold in biopsies from 2020 onward compared to prior decades, though further research is needed to confirm etiology. In 2025, a systematic review synthesized 19 cases from 1999 to 2024 across 16 studies, underscoring the condition's rarity and persistent association with allergic mechanisms. A significant milestone in understanding plasma cell gingivitis was the resolution of initial diagnostic uncertainties regarding its malignant potential. Early histopathological findings of massive plasma cell infiltrates often mimicked plasma cell neoplasms, prompting concerns for ; however, demonstrations of polyclonal (rather than monoclonal) plasma cell populations via confirmed its benign, inflammatory nature. This distinction, solidified through advancing immunohistochemical techniques in subsequent decades, shifted perceptions from potential oncologic threat to a treatable disorder.

Clinical Presentation

Signs and Symptoms

Plasma cell gingivitis primarily manifests as generalized and of the attached gingiva, often presenting with a bright, fiery coloration that sharply demarcates at the mucogingival junction. The gingival tissue exhibits mild enlargement, a friable or granular texture, and loss of normal , affecting the marginal, papillary, and attached regions without involvement of deeper periodontal structures. In most cases, the condition diffusely involves the anterior , particularly teeth 13-23, with occasional extension to the mandibular anterior segment (teeth 33-43), and no formation of periodontal pockets or attachment loss. swelling may occur in some patients, contributing to aesthetic concerns. Patients commonly experience easy on slight provocation, such as during brushing or probing, due to the highly inflamed and edematous nature of the gingiva. Symptoms are often mild, including occasional pain or a burning sensation triggered by spicy foods or certain toothpastes, though the condition can be , especially in areas of solitary red lesions. This inflammation arises from dense infiltration in the gingival tissues. Case examples illustrate these features across age groups. In adults, a 29-year-old presented with profuse on minimal provocation, redness, and gradual swelling in the anterior and mandibular gingiva, leading to poor esthetics. Similarly, a 57-year-old male reported discomfort and during brushing, with polypoid, erythematous, and edematous lesions in the anterior . In children, a 13-year-old exhibited a bright red, slightly elevated plaque on the anterior gingiva, with occasional swelling, , and but otherwise presentation. Pediatric cases around ages 7-10, as part of broader studies on young patients (mean age 11 years), show gingival with and mild , often responsive to hygiene measures. These manifestations are consistently verified through histological examination confirming predominance.

Clinical Variants

Plasma cell gingivitis primarily manifests in a gingival form, characterized by isolated involvement of the free and attached gingiva, presenting as diffuse and without extension to other oral sites. While PCG is confined to the gingiva, related conditions under the broader term plasma cell mucositis may involve other sites. Plasma cell affects the lips, typically appearing as circumscribed dark red plaques or erosive patches, predominantly the lower lip in elderly patients. Plasma cell involves the , featuring red, edematous, and sometimes eroded patches that may cause discomfort or . Plasma cell gingivostomatitis describes a multifocal presentation affecting the , , and broader , often as a triad of , , and . All these presentations share a common histopathological feature of dense polyclonal infiltration in the , though they differ primarily in the predominant anatomical sites of involvement.

and Pathogenesis

Causes

Plasma cell gingivitis is primarily attributed to a reaction triggered by exposure to specific antigens, leading to an inflammatory response in the gingiva. This immune-mediated process involves T-cell activation against the offending agent, resulting in dense infiltration without evidence of or in most instances. Common allergens implicated in this hypersensitivity include flavoring agents and spices such as cinnamonaldehyde and , often found in toothpastes, chewing gums, and lozenges. For example, multiple case reports have documented resolution of symptoms following discontinuation of cinnamon-containing herbal toothpastes or mint-flavored products, highlighting the direct causal role of these substances. Similarly, exposure to strong spices like red pepper or herbal ingredients in oral care products has been linked to onset in affected individuals. In addition to these primary triggers, other factors such as certain flavorings and herbal products contribute to cases of plasma cell gingivitis. A subset of cases remains idiopathic, with no identifiable despite thorough investigation. Some studies suggest that "plasma cell gingivitis" may encompass multiple entities, including reactive cases associated with drug exposures or underlying . A 2025 systematic review of 19 documented cases confirmed that etiologic factors were predominantly hypersensitivity-related, with symptom improvement upon avoidance in the majority.

Pathophysiology

Plasma cell gingivitis arises from an antigen-triggered that drives the differentiation of B cells into plasma cells, resulting in a dense subepithelial infiltration within the gingival . This process is characterized by a reaction, where exposure to allergens or irritants activates B lymphocytes, leading to their proliferation and maturation into antibody-secreting plasma cells. Pro-inflammatory cytokines, such as IL-6 and TNF-α, mediate this B-cell activation and recruitment, contributing to the localized accumulation of plasma cells without systemic involvement. Histologically, the condition features polyclonal aggregates of plasma cells in the , often organized into nodular collections separated by fibrous septa, with no evidence of cellular or . These plasma cells exhibit normal morphology, including eccentrically placed nuclei and abundant , and demonstrate polytypic expression of immunoglobulin light chains ( and ) in equal proportions, confirming their polyclonal nature. This infiltration is accompanied by a mixed inflammatory response involving T lymphocytes (CD3-positive) and occasional , but spares deeper periodontal structures. The inflammatory cascade in plasma cell gingivitis involves release that promotes , , and epithelial , manifesting as without associated loss or attachment apparatus destruction. Unlike neoplastic processes, the absence of light chain restriction and for monoclonal markers (e.g., no kappa/lambda imbalance) via distinguishes this benign reactive condition from plasma cell dyscrasias such as or . This polyclonal profile underscores the reactive, non-malignant etiology driven by persistent antigenic stimulation.

Diagnosis

Clinical Assessment

The clinical assessment of plasma cell gingivitis begins with a thorough evaluation to establish the , emphasizing the differentiation from plaque-induced and other inflammatory conditions. Accurate clinical evaluation is essential, as the condition mimics periodontitis and inflammatory but does not respond to standard periodontal therapy. A detailed and dental history is crucial, focusing on the onset and progression of symptoms such as gingival swelling and , often insidious over months. Inquiry into potential exposures includes allergens like toothpastes, gums, foods (e.g., , ), and herbal products (e.g., ), alongside a comprehensive history to identify triggers. Systemic illnesses, recent dental procedures, and practices are assessed to rule out plaque-induced , with minimal plaque accumulation typically noted in affected cases. Physical examination involves of the gingiva, which characteristically presents as bright red, edematous, and friable, with loss of and exaggerated contours, predominantly affecting the anterior and marginal, papillary, and attached regions. Probing reveals bleeding on slight provocation but shallow or absent periodontal pockets, indicating no significant attachment loss. Systemic signs, such as or skin lesions, are evaluated to exclude broader involvement, though patients are often systemically healthy. Laboratory investigations support the clinical findings by excluding systemic disorders. , including differential leukocyte count, , and platelet levels, is performed to rule out or other hematologic malignancies. and immunoglobulin levels (e.g., IgE, IgG) help exclude or , with normal results typical in plasma cell gingivitis. Additional tests, such as blood glucose, coagulation profile, and allergy-specific assays (e.g., skin prick or serum IgE for suspected allergens), may be indicated based on history. Differential diagnosis during assessment prioritizes ruling out conditions like , , autoimmune bullous diseases, and through the combined history, examination, and labs, ensuring plasma cell gingivitis is confirmed only after these exclusions.

Histopathological Findings

Histopathological examination of gingival biopsies in plasma cell gingivitis characteristically reveals a dense, band-like infiltrate of mature plasma cells within the juxtaepithelial , often comprising the predominant inflammatory component. These plasma cells may form aggregates containing , which are round, eosinophilic intracytoplasmic inclusions resulting from immunoglobulin accumulation. The overlying typically exhibits acanthosis with elongated rete ridges and , but lacks , ulceration, granulomas, or . Immunohistochemical analysis confirms the reactive, polyclonal nature of the plasma cell population, with equal expression of kappa and lambda light chains in an approximate 1:1 ratio and no evidence of light chain restriction. Plasma cells stain positively for CD138 and MUM1/IRF4, while remaining negative for and typically CD56, distinguishing the infiltrate from neoplastic processes. Under light microscopy at high magnification (e.g., ×400–×450), the s appear as round to oval cells with eccentric, clock-face nuclei, abundant basophilic , and occasional perinuclear halos, without cytologic or nodular architecture. is essential for definitive diagnosis, as it provides confirmatory tissue evidence of this non-neoplastic proliferation and enables exclusion of mimics such as plasma cell lymphoma through polyclonality and absence of aberrant immunophenotypic features.

Classification

Plasma cell gingivitis (PCG) is a benign, non-neoplastic condition primarily classified based on its into two main categories: allergic or -related and idiopathic or of unknown origin. Although an earlier classification from included a neoplastic category, contemporary understanding emphasizes that PCG features polyclonal infiltration and requires exclusion of neoplastic processes, such as or , which may present similarly but involve monoclonal proliferations. The allergic type, which is the most common, arises from reactions to external antigens such as flavored toothpastes, chewing gums, mouth rinses, or spices, leading to a benign inflammatory response characterized by polyclonal infiltration. The idiopathic form occurs without identifiable triggers or systemic associations, though it shares similar clinical and histological features with the allergic type. Classification can also be approached based on the site of involvement, with the core presentation limited to the gingiva in classic PCG, but extensions to adjacent mucosal sites defining related variants. These include plasma cell cheilitis affecting the lips, involving the tongue, and of the broader , often collectively termed plasma cell gingivostomatitis when multiple sites are affected. Regarding neoplastic potential, PCG is overwhelmingly benign and nonneoplastic, with the vast majority of cases representing reactive rather than ; however, rare instances may signal underlying with potential for progression to , underscoring the need for systemic evaluation in atypical presentations. A 2025 systematic highlights the predominance of mechanisms in confirmed PCG cases, reinforcing the etiologic focus on allergic triggers while emphasizing diagnostic vigilance for neoplastic exclusions. While primarily gingival, PCG may present with anatomical variants extending to or , as explored in clinical variants.

Management

Treatment Approaches

The primary treatment for plasma cell gingivitis involves identifying and discontinuing exposure to causative agents, such as cinnamon-flavored products, herbal toothpastes containing allergens like , or other irritants like leaves, which often leads to resolution within weeks to months. In a of 19 histopathologically confirmed cases, discontinuation of etiologic factors was a cornerstone modality, contributing to remission where allergens were successfully removed. This approach is particularly effective in hypersensitivity-related cases, emphasizing the need for detailed patient history to pinpoint triggers. Pharmacologic management typically begins with topical corticosteroids, such as 0.05% applied twice daily, which reduces inflammation and lesion severity in most patients. For refractory cases, topical 0.1% ointment serves as an effective alternative, achieving comparable pain reduction and lesion improvement to clobetasol, with mild side effects like transient burning. Systemic corticosteroids, such as (50 mg/day, tapered over weeks), or immunosuppressants like may be employed for severe or persistent disease, though complete remission rates remain low at about 10% without adjuncts. Antihistamines and antibiotics (e.g., 100 mg twice daily for 14 days) are sometimes added for symptom control. For lesions unresponsive to conservative measures, surgical excision via offers high efficacy, yielding complete remission in up to 88.9% of cases. Photobiomodulation therapy has emerged as a non-invasive adjunct, applied in select cases from the aforementioned 2025 review of 19 patients to promote healing alongside topical treatments. Throughout management, rigorous maintenance, including 0.2% mouthwashes and plaque control, is essential to prevent secondary and support recovery.

Prognosis

Plasma cell gingivitis is generally considered a benign condition with a favorable , particularly when the underlying trigger, such as an , is identified and eliminated, leading to complete resolution in most cases. In a series of 45 patients, approximately 55.6% achieved resolution with first-line therapy including and topical corticosteroids, while additional systemic treatments were required for persistent cases, with overall low rates of at 11.1%. Discontinuation of the offending agent, such as flavored toothpastes or herbal products, results in high success rates, often with symptom improvement within weeks. Recurrence is uncommon if the causative factor is fully avoided, though it may occur with re-exposure, emphasizing the importance of and avoidance. In idiopathic or allergic variants, the is excellent, with no evidence of or association with systemic plasma cell disorders like . Rare complications include persistent inflammation if untreated, potentially leading to gingival or discomfort, but neoplastic progression is not observed in non-neoplastic forms. Surgical interventions, such as , demonstrate quick healing, with resolution typically within 10 days to weeks post-procedure in responsive cases. Long-term follow-up, recommended for 6-12 months or longer based on clinical response, involves regular monitoring to ensure stability and detect any rare relapses early.

Epidemiology

Demographics

Plasma cell gingivitis affects individuals across a broad age spectrum, with reported cases ranging from 9 to 64 years and a mean age of approximately 28 years. The condition occurs in both pediatric and adult populations, though it remains rare overall. Females are disproportionately affected, comprising about 68% of cases compared to 32% in males, as evidenced by a of 19 cases that included 13 females and 6 males. No strong ethnic or racial predisposition has been identified in the literature on plasma cell gingivitis. The condition typically presents in otherwise healthy individuals without underlying systemic diseases.

Distribution and Risk Factors

Plasma cell gingivitis is a rare condition, with only sporadic cases reported in the literature and very few documented annually across medical centers. For instance, a single-institution study over two decades identified just 45 cases, underscoring its infrequency. Plasma cell cheilitis, a related variant affecting the , is even rarer and often overlaps with gingival involvement in contexts. Large-scale epidemiological data on prevalence are lacking due to the condition's rarity, but it is estimated to account for less than 1% of gingival diseases based on biopsy analyses. In one retrospective review of over 1,500 biopsied gingival lesions, plasma cell gingivitis represented approximately 0.5% of cases. The gingival form universally involves the anterior maxilla, with lesions typically presenting as diffuse, erythematous swelling in this region. Key risk factors include exposure to allergens such as flavorings in , toothpastes, and certain foods, which trigger reactions leading to infiltration. A possible atopic predisposition has been suggested in some patients with underlying tendencies, though this association remains unconfirmed in broader cohorts. No strong genetic links have been identified, with the condition appearing idiopathic in most instances. Reports of plasma cell gingivitis peaked in the late and early , largely attributed to allergic reactions to specific ingredients like in , with clusters of cases documented during that period. Incidence has since decreased, likely due to formulation changes in consumer products to remove common allergens, though isolated cases continue to be reported globally. There is a noted female predominance in affected individuals.

References

  1. https://pmc.ncbi.nlm.nih.gov/articles/PMC9362808/
  2. https://pmc.ncbi.nlm.nih.gov/articles/PMC4439636/
  3. https://pubmed.ncbi.nlm.nih.gov/40252807/
  4. https://www.mdpi.com/2039-7283/15/9/158
  5. https://journals.lww.com/aomr/fulltext/2014/26050/plasma_cell_gingivitis__a_case_report.4.aspx
  6. https://pmc.ncbi.nlm.nih.gov/articles/PMC9581649/
  7. https://www.pathologyoutlines.com/topic/oralcavityplasmacellgingivitis.html
  8. https://pubmed.ncbi.nlm.nih.gov/5259736/
  9. https://pubmed.ncbi.nlm.nih.gov/5285187/
  10. https://www.sciencedirect.com/science/article/abs/pii/0030422081900384
  11. https://www.researchgate.net/publication/368551104_Plasma_Cell_Gingivitis_and_Its_Mimics
  12. https://www.oooojournal.net/article/S2212-4403(23)00642-9/abstract
  13. https://www.cureus.com/articles/376774-atypical-gingivitis-a-rare-entity
  14. https://www.sciencedirect.com/science/article/abs/pii/S2468785525001648
  15. https://onlinelibrary.wiley.com/doi/10.1155/2022/2992656
  16. https://www.researchgate.net/publication/11531587_Plasma_cell_gingivitis
  17. https://aap.onlinelibrary.wiley.com/doi/10.1902/jop.2011.100663
  18. https://exodontia.info/plasma-cell-gingivitis/
  19. https://pmc.ncbi.nlm.nih.gov/articles/PMC6433141/
  20. https://pmc.ncbi.nlm.nih.gov/articles/PMC7049820/
  21. https://pmc.ncbi.nlm.nih.gov/articles/PMC3742897/
  22. https://pmc.ncbi.nlm.nih.gov/articles/PMC8123247/
  23. https://pubmed.ncbi.nlm.nih.gov/37431113/
  24. https://doi.org/10.3390/jcm10040830
  25. https://pmc.ncbi.nlm.nih.gov/articles/PMC7922699/
  26. https://pmc.ncbi.nlm.nih.gov/articles/PMC5198463/
  27. https://jsstd.org/plasma-cell-gingivitis-an-enigma/
  28. https://pmc.ncbi.nlm.nih.gov/articles/PMC6942776/
  29. https://pmc.ncbi.nlm.nih.gov/articles/PMC3800421/
  30. https://pmc.ncbi.nlm.nih.gov/articles/PMC12468285/
  31. https://doi.org/10.1016/j.jormas.2025.102378
  32. https://pmc.ncbi.nlm.nih.gov/articles/PMC12388118/
  33. https://pmc.ncbi.nlm.nih.gov/articles/PMC12220169/
  34. https://pmc.ncbi.nlm.nih.gov/articles/PMC9626791/
  35. https://pmc.ncbi.nlm.nih.gov/articles/PMC11470447/
  36. https://dermnetnz.org/topics/plasma-cell-mucositis
  37. https://jamanetwork.com/journals/jamadermatology/fullarticle/533178
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