Increase in the size of the gingiva is a common feature of gingival disease. Accepted current terminology for this condition is gingival enlargement and gingival overgrowth. These are strictly clinical descriptive terms and avoid the erroneous pathologic connotations of terms used in the past such as hypertrophic gingivitis or gingival hyperplasia. The gingiva and associated soft tissues of the periodontium may be enlarged in response to various interactions between the host and the environment. Although such enlargement usually represents an inflammatory response to bacterial plaque, increased susceptibility as a result of systemic factors or conditions should always be considered during the course of patient evaluation. Systemically related gingival enlargements include, but are not limited to, scurvy, leukemia, puberty, pregnancy, multisystem syndromes and selected drugs and/or agents. In addition, fibrotic gingival enlargement has been reported and is believed to be the result of a genetic predisposition (for example hereditary or familial gingival enlargement). However an idiopathic variant that has not been associated with genetic linkage or cause has been described. Of the predisposing factors associated with the gingival enlargement, selected anticonvulsant drug, Calcium channel blockers and a potent immunosuppressant (Cyclosporine A) have generated the most investigative attention in the scientific community.
Since the first report of Phenytoin induced gingival overgrowth by Kimball in 1939, many clinical and investigative studies have been carried out to determine the pathogenesis of this disorder. Although these studies yielded various pathogenetic data, it is still unknown why drugs with such different pharmacological actions induce similar gingival changes. Furthermore different views concerning the interrelationships between blood drug levels and/or duration of drug intake and the severity of growth, sex predilection, effect of local inflammation and incidence has been reported in the literature.
The genetically determined capacity of the host to deal metabolically with chronically administered drugs; the responsiveness of gingival tissues to the drugs and the pre-existing gingival condition may differ among individuals.
Inhaltsverzeichnis (Table of Contents)
- Introduction
- Classification
- Review of Literature
- GENERAL INFORMATION
- Clinical Features
- Histopathology
- THE MECHANISM OF DRUG-INDUCED GINGIVAL OVER GROWTH
- Historical perspective
- Review of Hypothesis
- Inflammation from bacterial plaque
- Increased Sulfated Glycosaminoglycans (GAGs)
- IMMUNOGLOBULINS
- Gingival fibroblast phenotype population differences
- Epidermal Growth Factor (EGF)
- Pharmacokinetics and tissue – binding
- Collagenase activation
- Disruption of fibroblast cellular Na+ /Ca2+ flux
- Folate
- A Combination hypothesis
- Risk Factors for drug – induced gingival overgrowth
- Age and other Demographic variables
- Drug Variables
- Concomitant Medication
- Periodontal variables
- Genetic factors
- In Vitro Studies
- A Review of studies in the Rat model
- Drug Dose and blood levels
- Duration of drug administration
- Sex
- Age
- Dental Plaque
- Similarities in Other Animal Models
- Table – Drugs associated with gingival overgrowth
- Anticonvulsants
- PHENYTOIN
- History
- Structure – Activity Relationship
- Clinical Manifestation
- PHARMACOKINETICS
- Pathogenesis
- In vitro studies
- HISTOLOGICAL CHARACTERISTICS
- Prevention and treatment
- Other anticonvulsant agents that have been associated with gingival overgrowth
- Vigabatrin induced gingival overgrowth
- IMMUNOSUPPRESSANTS
- Cyclosporin induced gingival overgrowth
- Pharmacokinetics
- Clinical manifestations
- Pathogenesis of gingival overgrowth
- HISTOLOGICAL CHARACTERISTICS
- Prevention and the role of inflammation
- Tacrolimus
- CALCIUM CHANNEL BLOCKERS
- Pharmacokinetics
- Dihydropyridines
- Clinical manifestations
- Pathogenesis
- Histological characteristics
- Prevention and treatment
- Other calcium channel blockers
- Table II 000 95:79:715-22
- New clinical index for gingival overgrowth
- Grade0
- Grade1
- Grade2
- Grade3
- Grade4
- Treatment options
- Decision tree for the treatment of drug-induced gingival overgrowth
- Maintenance
- Gingivectomy
- The Flap Technique
- Table 1. Drugs associated with gingival overgrowth
- Bibliography
- The causes and clinical features of drug-induced gingival enlargement
- The various drugs associated with the condition, including anticonvulsants, immunosuppressants, and calcium channel blockers
- The complex mechanisms underlying the pathogenesis of drug-induced gingival enlargement, focusing on the role of inflammation, fibroblast heterogeneity, and growth factors
- The role of genetic factors in determining individual susceptibility to drug-induced gingival enlargement
- The prevention and treatment strategies for drug-induced gingival enlargement, including plaque control, surgical interventions, and drug management
Zielsetzung und Themenschwerpunkte (Objectives and Key Themes)
This text provides a comprehensive review of drug-induced gingival enlargement, exploring its causes, clinical manifestations, pathogenesis, and treatment options. The text focuses on the various factors involved in the condition, including drug variables, inflammatory processes, and genetic predispositions. It examines the mechanisms of drug-induced gingival overgrowth, with a particular emphasis on the roles of fibroblasts, growth factors, and collagen metabolism.Zusammenfassung der Kapitel (Chapter Summaries)
The first section introduces the topic of drug-induced gingival enlargement, providing a historical perspective and a detailed classification system for the condition. The subsequent section delves into the review of literature, summarizing existing knowledge on the clinical features, histopathology, and proposed mechanisms of drug-induced gingival enlargement. This section provides a comprehensive overview of various hypotheses related to the condition, encompassing bacterial inflammation, increased glycosaminoglycans, immunoglobulins, fibroblast phenotype differences, epidermal growth factor, pharmacokinetics and tissue binding, collagenase activation, disruption of cellular sodium/calcium flux, folate, and a combination hypothesis. The text then explores the various risk factors associated with drug-induced gingival enlargement, including age, gender, drug dosage and concentration, concomitant medications, periodontal variables, and genetic factors. Further, the text provides insights into the in vitro studies conducted to investigate the cellular and molecular mechanisms of drug-induced gingival enlargement, emphasizing the role of fibroblasts, growth factors, and collagen metabolism. The final section presents a comprehensive review of the rat model, a commonly used animal model for investigating drug-induced gingival enlargement. The rat model allows researchers to explore the effects of various drugs, dosage, duration of administration, sex, age, and dental plaque on the development of gingival overgrowth.Schlüsselwörter (Keywords)
The main focus of this text lies on drug-induced gingival enlargement. The primary keywords include: drug-induced gingival overgrowth, gingival enlargement, gingival hyperplasia, anticonvulsants, immunosuppressants, calcium channel blockers, Phenytoin, Cyclosporine A, Nifedipine, fibroblasts, growth factors, collagen metabolism, inflammation, genetic factors, prevention, and treatment.- Quote paper
- Dr. Rajesh Hosadurga (Author), 2005, Drug Induced Gingival Enlargement, Munich, GRIN Verlag, https://www.grin.com/document/215797
