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| CASE REPORT |
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| Year : 2019 | Volume
: 9
| Issue : 1 | Page : 44-47 |
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Interdisciplinary approach in the management of medically compromised patient with drug-induced gingival enlargement
Archana Devanoorkar1, Nagappa Guttiganur2
1 Department of Dentistry, Gulbarga Institute of Medical Sciences, Gulbarga, Karnataka, India
2 Department of Periodontics, AME'S Dental College and Research Centre, Raichur, Karnataka, India
| Date of Web Publication | 18-Feb-2019 |
Correspondence Address:
Archana Devanoorkar
Department of Dentistry, Gulbarga Institute of Medical Sciences, Gulbarga, Karnataka
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jid.jid_68_17
 Abstract | | |
Drug-induced gingival overgrowth (DIGO) is one of the most common side effects of three important groups of drugs such as anticonvulsants, calcium channel blockers, and immunosuppressants. Calcium channel blockers are the important group of drugs in the management of cardiovascular diseases; however, they are associated with certain side effects such as DIGO in susceptible individuals. Nifedipine is the frequently involved drug; however, there are few cases of amlodipine-induced gingival enlargement as well. The case reported here is a 55-year-old medically compromised male patient on polypharmacy. Based on the clinical, radiographic investigations and medical history, he was diagnosed as having drug-induced gingival enlargement with chronic generalized periodontitis. The case was managed by nonsurgical periodontal therapy alone in addition to interdisciplinary approach and strict supportive periodontal therapy, which resulted in complete resolution of the gingival enlargement with restoration of normal gingival health.
Keywords: Drug-induced gingival enlargement, interdisciplinary approach, nonsurgical periodontal therapy, polypharmacy
How to cite this article:
Devanoorkar A, Guttiganur N. Interdisciplinary approach in the management of medically compromised patient with drug-induced gingival enlargement. J Interdiscip Dentistry 2019;9:44-7 |
How to cite this URL:
Devanoorkar A, Guttiganur N. Interdisciplinary approach in the management of medically compromised patient with drug-induced gingival enlargement. J Interdiscip Dentistry [serial online] 2019 [cited 2023 Mar 30];9:44-7. Available from: https://www.jidonline.com/text.asp?2019/9/1/44/252530 |
| Clinical Relevance to Interdisciplinary Dentistry | |  |
The case reported here was managed with regular SPT. Interdisciplinary approach played an important role in the rehabilitation of Patient to restore the mastication, Phonetics and esthetics.
| Introduction | | |
Gingival overgrowth is one of the most common oral side effects of many of the systemically administered drugs, in susceptible individuals.
It was first observed in patients who were on phenytoin for epilepsy, with approximately 50% having gingival overgrowth. Cyclosporine is an immunosuppressant which has been reported to cause gingival enlargement in 25%–80% of patients.[1] Dihydropyridines (e.g., nifedipine, felodipine, and amlodipine) tend to be more commonly associated with gingival enlargement than the other subgroups of calcium channel antagonists.
“Gingival hyperplasia” and “gingival hypertrophy,” the earlier terms for increase in the gingival size, have been replaced by the term gingival overgrowth/enlargement as the previous terms did not accurately reflect the histologic composition of the pharmacologically modified gingiva. Currently, more than 20 prescription medications are associated with gingival enlargement.[2]
Drugs associated with gingival enlargement can be broadly divided into three categories: anticonvulsants, calcium channel blockers, and immune suppressants. Of this large group of drugs, the dihydropyridines are the agents most frequently implicated.[3]
Amlodipine, a newer agent of dihydropyridine, used for the treatment of hypertension and angina, was first reported for causing gingival overgrowth as side effect, by Seymour et al. in 1991.[4]
Pathogenesis
A number of factors affect the relationship between drug and gingival overgrowth. Pathogenesis of drug-induced gingival enlargement appears to be of multifactorial origin with no satisfying unifying hypothesis. Many factors are involved in the etiology and pathogenesis of drug-induced gingival overgrowth (DIGO) that can be broadly categorized as patient-related and drug-related factors.
Patient-related factors include age, gender, and oral hygiene. Plaque scores and gingival inflammation appear to exacerbate the expression of DIGO, irrespective of the initiating drug.[4]
There is a variable gingival response in patients taking these drugs; hence, the term responders and nonresponders are being used to describe the patient susceptibility to drugs. Age has been reported as a risk factor for phenytoin- and cyclosporine-induced gingival overgrowth; however, it is not an applicable risk factor for the calcium channel blockers since the use of these drugs is usually confined to the middle-aged and older adult.[5]
Genetic factors also have an influence on the DIGO. Fibroblast heterogeneity remains one of the key factors used to explain the variable response of the gingival tissues to the various drugs inducing gingival overgrowth. One genetic marker that has been investigated in relation to DIGO is the human lymphocyte antigen (HLA) expression. A study reported that patients who expressed HLA-DR1 are afforded some degree of protection against gingival overgrowth while HLA-DR2 may increase the development of this unwanted effect.[6]
Other factors that have been studied in association with DIGO are fibroblast phenotype, growth factors, and cytokines.
Fibroblast phenotype
Gingival enlargement is not seen in all the participants on calcium channel blockers but only seen in susceptible individuals. Hence, it has been hypothesized that these individuals have fibroblasts with an abnormal susceptibility to the drug. It also has been proposed that susceptibility or resistance to pharmacologically induced gingival enlargement may be governed by the existence of differential proportions of fibroblast subsets in each individual which exhibit a fibrogenic response to this medication.[7]
Growth factors and cytokines
Platelet-derived growth factor and fibroblast growth factors are proposed to enhance the cell proliferation and thus induce the DIGO. A synergistic enhancement of collagenous protein synthesis by human gingival fibroblasts was found when these cells were exposed to nifedipine and interleukin-1b (IL-1b), a pro-inflammatory cytokine that is elevated in inflamed gingival tissues.[8] IL-1b and IL-6 may play a role in the fibrogenic responses of the gingiva to these medications.[9]
Because most types of pharmacological agents implicated in gingival enlargement have negative effects on calcium ion influx across cell membranes, it was postulated that such agents may interfere with the synthesis and function of collagenases.[10]
Prevention and management of drug-induced gingival overgrowth
Meticulous plaque control by home care and professional care measures, and regular periodontal maintenance therapy, periodic checkup with necessary scaling, root planing, and elimination of plaque retentive factors are the measures that could be undertaken to prevent DIGO. However some cases may require drug substitution in addition to periodontal therapy.
Treatment
Treatment of DIGO can be broadly categorized into nonsurgical and surgical intervention methods.
Nonsurgical therapy encompasses scaling, root planing, elimination of plaque retentive factors, adequate home care measures for plaque control, and close monitoring of the patient at regular intervals. Drug substitution is also one of the alternative methods.
Surgical intervention
When a patient does not respond to nonsurgical therapy or if it recurs following nonsurgical therapy, such cases may require surgical intervention. Internal bevel gingivectomy or external bevel gingivectomy is the treatment of choice depending on the type of the case.
Medically compromised patients in whom the surgical intervention cannot be considered because of their underlying systemic health, nonsurgical therapy and or drug substitution only is the alternative in addition to strict supportive periodontal therapy (SPT) and close monitoring. One such case is reported here.
| Case Report | | |
A 55-year-old male patient reported to the Department of Periodontics, The Oxford Dental College, Hospital and Research Center, Bangalore, with the chief complaint of swollen gums involving both upper and lower teeth [Figure 1] and [Figure 2] and loose tooth in the upper front region. Medical history revealed that he was diabetic and hypertensive for 10 years, and also had undergone angioplasty 10 years back. Drug history revealed that he was on multiple drugs that included glibenclamide 5 mg/day, amlodipine 5 mg/day, ecosprin 150 mg/day, and statins 10 mg/day. Periodontal examination showed generalized periodontal pockets with attachment loss ranging from 5 mm to 7 mm. He had a poor oral hygiene with generalized gingival enlargement and generalized gingival inflammation.
Radiographic examination
Orthopantomograph revealed the presence of generalized horizontal bone loss with circumferential bone loss in relation with (irw) 18 and 26 root stump [Figure 3]. Complete hemogram was done, and all the parameters were within normal ranges.
Based on clinical, radiographic features and medical history, the diagnosis of generalized chronic periodontitis with drug-induced gingival enlargement was done.
| Discussion | | |
The treatment planned was extraction of teeth with hopeless prognosis (18 and 26) in the emergency phase followed by nonsurgical periodontal therapy that included scaling, root planing, supra- and subgingival irrigation with chlorhexidine, and elimination of all the plaque retentive areas, oral hygiene instructions were given, and the patient was put under strict SPT every month for initial 3 months followed by every 3 months during next 1 year.
During SPT, he presented with periodontal abscess irw 11, so it was considered for extraction. However, other areas with extensive gingival enlargement and exudation showed drastic improvement at the end of 1 year. The patient was followed up further, and a fixed prosthesis was planned irw all the missing teeth, i.e., 26, 11. Since there was a drastic improvement in the periodontal status from baseline, with reduction of probing depth to 2–3 mm, and the patient was compliant with strict maintenance therapy, surgical intervention was not considered. There was complete resolution of gingival enlargement with restoration of normal gingival architecture [Figure 4]. | Figure 4: Posttreatment follow-up of 2 years with restoration of normal periodontal health
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| Conclusion | | |
Continued clinical research and advancement in the field of periodontics have been replacing the previous treatment modalities such as scaling and root planing with the more advanced techniques such as gene therapy and much more. However, it is the clinician who has to be wise and more challenging to tailor the treatment as per the case demand. In spite of the vast advancements, in few cases as mentioned in the above case report, wherein more aggressive methods cannot be adopted because of the underlying systemic conditions, nonsurgical therapy still holds the gold standard. Close monitoring and continued patient motivation and education in addition to SPT have given the best results in the above case. Interdisciplinary approach in the case management benefitted the patient by restoring the esthetics, phonetics, and mastication.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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| 2. | Rees TD, Levine RA. Systemic drugs as a risk factor periodontal disease initiation and progression. Compend Contin Educ Dent 1995;16:20-42. |
| 3. | Seymour RA, Ellis JS, Thomason JM, Monkman S, Idle JR. Amlodipine-induced gingival overgrowth. J Clin Periodontol 1994;21:281-3. |
| 4. | Seymour RA. Calcium channel blockers and gingival overgrowth. Br Dent J 1991;170:376-9. |
| 5. | Ellis JS, Seymour RA, Steele JG, Robertson P, Butler TJ, Thomason JM, et al. Prevalence of gingival overgrowth induced by calcium channel blockers: A community-based study. J Periodontol 1999;70:63-7. |
| 6. | Pernu HE, Knuuttila ML, Huttunen KR, Tiilikainen AS. Drug-induced gingival overgrowth and class II major histocompatibility antigens. Transplantation 1994;57:1811-3. |
| 7. | Hassell TM, Page RC, Narayanan AS, Cooper CG. Diphenylhydantoin (dilantin) gingival hyperplasia: Drug-induced abnormality of connective tissue. Proc Natl Acad Sci U S A 1976;73:2909-12. |
| 8. | Johnson RB, Zebrowski EJ, Dai X. Synergistic enhancement of collagenous protein synthesis by human gingival fibroblasts exposed to nifedipine and interleukin-1-beta in vitro. J Oral Pathol Med 2000;29:8-12. |
| 9. | Williamson MS, Miller EK, Plemons J, Rees T, lacopino AM. Cyclosporine A up regulates interleukin-6 gene expression in human gingiva: Possible mechanism for gingival overgrowth. J Periodontol 1994;11:552-60. |
| 10. | Hassell TM. Evidence for production of an inactive collagenase by fibroblasts from phenytoin-enlarged human gingivae. J Oral Pathol 1982;11:310-7. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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