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GINGIVAL HYPERPLASIA

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  • 21/02/2012 at 4:40 pm #10354
    drsushant
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    A case report and literature review by Ahmad et al investigated a possible dose-related case of gingival hyperplasia in a child receiving the drug amlodipine. A 9-year-old girl was presented to the hospital with a history of membranous ne­phro­pathy and hypertension, and was unable to gain weight. She was allergic to the drug enalapril and had gingival hyperplasia. Her medication profile revealed that amlodipine and azathioprine were possible agents for the gingival hyperplasia, and the child’s mother had observed the hyperplasia following an increase in the dosage of amlodipine. After being discharged from the hospital, the patient could no longer eat by mouth and her gums bled upon brushing. The authors reviewed the literature regarding the use of amlodipine in children, and a subsequent review found one animal study that showed a relationship between amlodi­pine dose/plasma concentration and gingival hyperplasia. This relationship was reported in humans with other calcium channel blockers, but not with amlodi­pine and not in a child. The Naranjo probability scale revealed a possible adverse reaction of gingival hyperplasia associated with amlodipine. The authors state that, to their knowledge this is the first report of a possible dose-related occurrence of gingival hyperplasia in a child receiving amlodipine.

            

    21/02/2012 at 4:41 pm #15203
    drsushant
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     Gingival hyperplasia involves the excessive growth of either the epithelial tissue that lies on the surface of the gums or the connective tissue that lies beneath the surface. Prickle cells proliferate, and rete ridges become abnormally long. Prickle cells are rough-looking cells that normally form an orderly layer in the epidermis. Rete ridges are epidermal cells that jut into the dermal layer beneath it. Such irregularities in the gum tissue provide havens for bacterial growth, and complications may result, such as the inflammation of the gums known as gingivitis. Enlargement of gingival tissue also causes emotional distress and adversely affects facial appearance of people of all ages. Young children may experience difficulties when new teeth breaking through the gums.
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    Congenital Gingival Hyperplasia
    In some cases, children suffer congenital gingival hyperplasia. This means that the condition exists when the child is born. The condition is often associated with some other congenital abnormality, such as hypertrichosis, a condition in which body hair grows in abundance.
    Diseased-Induced Gingival Hyperplasia
    People of all ages, including children, may suffer gingival hyperplasia as a result of some systemic diseases. The "European Journal of Dentistry" reports a case in which gingival hyperplasia proved to be a symptom of a cancerous condition called acute myeloblastic leukemia. Since excessive gingival growth is an early symptom of the disease, its presence in the patient gave timely warning to the serious underlying disease. Prompt treatment of the leukemia resulted in an amelioration of the gingival disorder. Other similar forms of leukemia also cause gingival hyperplasia, such as myelomonocytic leukemia.
    Drug-Induced Gingival Hyperplasia
    Gingival hyperplasia may result from the use of prescription medicines such as cyclosporine, a drug that depresses the immune system, and amlodipine, a calcium-blocking drug given to patients suffering hypertension. Phenytoin, a drug used to treat epilepsy, causes an especially large number of gingival hyperplasia cases. Children suffer this side effect more frequently than adults, and boys suffer more frequently than girls. Discontinuance of phenytoin reverses the condition but does not completely cure it.

     

            

    21/02/2012 at 4:45 pm #15204
    drsushant
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     Gingival overgrowth is an important adverse effect of phenytoin (PHT) therapy, occurring in about half of the patients. This study aimed to evaluate the effect of oral folic acid supplementation (0.5 mg/day) for the prevention of PHT-induced gingival overgrowth (PIGO) in children with epilepsy aged 6-15 years on PHT monotherapy for 6 months.

    METHODS:

    This was a randomized, double-blind, placebo-controlled trial conducted at a tertiary level hospital from May 2008 to June 2009. Children aged 6-15 years started on PHT monotherapy within last 1 month were eligible for inclusion. Preexisting gingival overgrowth, use of other folic acid antagonists, and macrocytic anemia were exclusion criteria. Trial subjects were randomized to receive either folic acid or placebo. The primary outcome measure was incidence of any degree of gingival overgrowth after 6 months of PHT monotherapy. The trial was registered with clinicaltrials.gov (NCT00781196).

    RESULTS:

    A total of 120 children were recruited, 62 and 58, respectively, in folic acid and placebo arms. The 2 arms were comparable at baseline. Twenty-one percent of patients in the folic acid arm developed PIGO, as compared with 88% receiving placebo (p < 0.001). Absolute risk reduction of PIGO by folic acid was 67% (95% confidence interval 54%-80%), and relative risk reduction was 0.76.

    CONCLUSIONS:

    Oral folic acid was found to decrease the incidence of PIGO in children on PHT monotherapy, in a statistically significant and clinically relevant manner. Classification of evidence: This study provides Class I evidence that folic acid supplementation, 0.5 mg/day, is associated with prevention of gingival overgrowth in children taking PHT monotherapy.

            

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