Gingival enlargements (GEs) are a commonly observed clinical entity in dentistry. The etiology maybe local, systemic, or a combination. Having a good diagnostic certainty of the type of GE helps the clinician to not only manage the entity locally but facilitates a thorough workup of the systemic factors. This article offers an in-depth look at the diagnosis and subsequent clinical management strategies for various forms of GE. It emphasizes the importance of accurately recognizing the diverse clinical presentations of GE, guided by its etiopathogenesis, clinical features, and other investigations. Achieving an accurate diagnosis is crucial for effective management.
Key points
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It is essential for clinicians to possess an in-depth awareness of the various forms of gingival enlargement (GE), given their significant impact on prognosis and patient outcomes.
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Dentists must acknowledge and address both the oral hygiene and psychological implications associated with GE by initiating timely and effective management strategies.
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Managing drug-influenced GE and GE secondary to systemic factors often requires a multidisciplinary approach. Therefore, clinicians should be cognizant of the importance of prompt referrals to physicians when indicated.
Abbreviations
| DIGE | drug-influenced gingival enlargement |
| GE | gingival enlargement |
Introduction
The term gingival enlargement (GE) refers to an increase in the gingival size. The condition is multifactorial. The various etiologic factors include genetics, medications, dental plaque, and systemic diseases, among others. , There appears to be considerable changes, and many times some level of confusion in the literature regarding the terminology. Terms such as gingival hyperplasia, gingival hypertrophy, drug-induced gingival hyperplasia, and other previous synonyms have been largely replaced in the literature by the term “GE”. Throughout this article, we have used the term GE to reflect the most current dental literature. In this article, we review the etiology, classification, pathophysiology, clinical features, differential diagnosis, management, and other factors as related to GE.
Terminology and classification
A universally acceptable succinct classification of GE is lacking in the existing literature. The lack of consensus in the related terminology and the various definitions used over the past several decades may have contributed to this shortcoming in the literature. It must be noted, however, that relative consensus can be found in the periodontal literature, especially the periodontal disease classifications of 1999 and 2017 by the American Academy of Periodontology. , To add to this apparent confusion, various textbooks recommended globally for dental undergraduate education, also show varying and dissimilar terminologies. Many times, the terms GE and gingival overgrowth also seem to be interchangeably used in these standard dental/periodontal textbooks. ,,, There is a current necessity for a universally acceptable classification of GE that can be a consensus among various dental specialties and related professional organizations. One of the most prevalent forms of GE is often associated with gingivitis-induced inflammation, more commonly seen in adolescents undergoing orthodontic treatment. ,
The second and the more diagnostically challenging form of the GE is drug-influenced gingival enlargement (DIGE). The systemic use of, primarily, 3 classes of drugs—anticonvulsants, calcium channel blockers, and immunosuppressants, have been identified in the causation of DIGE. , GE has also been associated with certain genetic conditions, systemic conditions, hormonal changes, or even neoplastic conditions. , A GE condition that cannot be attributed to any of the aforementioned causes, can be classified under idiopathic GE. Throughout the literature on classification of GE, there appears to be a significant lack of consensus between and among various professional organizations and specialty academies in dentistry.
Etiology, pathophysiology, and clinical features of common gingival enlargement
The distinct pathologic characteristics of all GEs, regardless of their cause, necessitate careful attention during diagnostic and therapeutic procedures, as well as during the maintenance. Recurrence is a significant concern, especially when systemic conditions are involved, making it vital to determine the etiology and any contributing factors. The more common GE entities are summarized in Table 1 .
Table 1
Etiology, pathophysiology, and clinical features of common gingival enlargement
| Category | Etiology | Pathogenesis | Clinical Features |
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| Inflammatory gingival enlargement , |
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| Drug-influenced gingival enlargement , |
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| Systemic conditions ,, |
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| Hereditary gingival fibromatosis ,, |
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Etiology, pathophysiology, and clinical features of uncommon gingival enlargement
Orthodontic appliances, fixed dental prostheses, and removable dentures each contribute to GE through unique mechanisms. These factors initiate a cascade of inflammatory and fibrotic changes within the gingival tissues, ultimately leading to distinct clinical presentation. The etiology, pathophysiology, and clinical features of these entities are summarized in Table 2 .
Table 2
Etiology, pathophysiology, and clinical features of uncommon gingival enlargement
| Category | Etiology | Pathogenesis | Clinical Features |
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| Orthodontic bracket/material related GE ,,,,,, |
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| GE related to fixed dental prosthesis ,,, |
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| GE related to removable prosthesis ,,, |
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| Peripheral giant cell granuloma ,,,,,, |
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GE can be classified based on various factors, including but not limited to etiology, tissue appearance, etiopathogenesis, location, and distribution among others. A brief summary of these classifications is depicted in Fig. 1 . ,
Classification of GE.
Diagnostic approaches
Thorough patient history and clinical examination are paramount. A photographic documentation, by means of pictures or intra-oral scans, may be beneficial for both patient education and prognosis assessment. Appropriate imaging followed by succinct laboratory/blood investigations should be ordered by the treating clinician. Tissue biopsy accompanied by histopathology may be warranted in certain cases. The most probable differential diagnoses, finally culminating in diagnosis proper, is instrumental in optimal management of GE. A diagnostic paradigm and a suggested sequential clinical approach are summarized in Fig. 2 .
Sequential diagnostic and management paradigm for GE.
Management strategies
Management strategies for GE primarily are based on etiology.
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Non-surgical management:
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Oral hygiene instructions
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Scaling and root planing
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Drug substitution (in drug-influenced cases)
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Management of underlying systemic conditions
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Surgical management:
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Gingivectomy/gingivoplasty
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Flap surgery
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Mucogingival/periodontal plastic surgery
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Laser gingivectomy
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Other modalities such as photobiomodulation therapy, host modulation therapy, and novel drug delivery systems.
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Management of plaque-induced GE is well documented in the literature, the pillar stones being meticulous plaque control and oral hygiene maintenance. For the management of DIGE, keeping plaque in check is essential, along with potential drug substitution following discussion with a physician. ,
Nifedipine, a known drug for GE, can be replaced by alternatives such as benidipine, nicardipine, or isradipine, which have not demonstrated an association with this condition. , In cases where complete resolution is not achieved, surgical intervention may become necessary.
In orthodontic-related GE, key interventions include reinforcing oral hygiene through the use of interdental brushes and antimicrobial mouth rinses, performing professional plaque removal, and modifying appliances to reduce mechanical irritation. , For patients with nickel sensitivity, switching to non-metallic alternatives is recommended. , When GE is linked to fixed prostheses, treatment focuses on correcting design flaws such as over-contouring or poor fit, maintaining optimal plaque control through regular dental visits, addressing any associated periodontal issues, and surgically excising fibrotic tissue when indicated. ,, For removable prosthesis-induced GE, management includes adjusting or replacing ill-fitting dentures, advising patients to remove prostheses overnight to facilitate tissue healing, improving hygiene with antifungal agents, if needed, and performing surgical excision of hyperplastic tissue in severe cases. ,,, A flow chart representing a sequential diagnostic and management paradigm is depicted in Fig. 2 .
If GE persists and/or recurs, surgical management may be considered. The various surgical modalities, along with their indications, advantages, and limitations have been listed in Table 3 .
Table 3
Surgical techniques for gingival enlargement: indications, advantages, and limitations
| Technique | Indications | Advantages | Limitations |
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| Gingivectomy , | Suprabony enlargement, no bone loss. |
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| Gingivoplasty | Contour sculpting, esthetic finishing. |
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| Flap surgery , | Pocket with bone loss/attachment loss. |
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| Mucogingival/periodontal plastic surgery , | Recession, keratinized tissue deficiency, esthetics. |
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| Laser gingivectomy , | Need for hemostasis, comfort, esthetics. |
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| Dual flap internal gingivectomy | DIGE and periodontitis |
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