ABSTRACT
Antecedentes: El agrandamiento gingival inducido por medicamentos es una condición clínica frecuente en pacientes que ingieren anticonvulsivos, inmunosupresores y bloqueadores de los canales de calcio. La prevalencia de agrandamiento gingival inducido por medicamentos es del 3 % al 20 % en el grupo de las condiciones gingivales inflamatorias. Todos estos medicamentos producen lesiones clínicas y características histológicas indistinguibles unas de otras, que llegan a afectar la función y la estética de los pacientes afectados. Objetivo: Describir el manejo terapéutico integral y el seguimiento a 12 meses de una paciente con agrandamiento gingival inducido por tacrolimus y amlodipino. Descripción del caso: Una mujer de 22 años con discapacidad mental limítrofe y receptora de trasplante renal se remitió al servicio de Odontología del Hospital Infantil Universitario de San José (Bogotá, Colombia) por presentar agrandamiento gingival. El examen clínico mostró un índice de placa de O'Leary del 84,3 %, in flamación generalizada y bolsas gingivales de 4-6 mm. El equipo de trasplante renal revisó el protocolo de tratamiento periodontal que incluyó: trabajo con la familia para red de apoyo, diseño de un programa personalizado de higiene oral, gingivectomía y mantenimientos periodontales periódicos. Esta estrategia terapéutica permitió reducir el índice de placa y lograr un resultado clínico favorable. Conclusión: La condición sistêmica y psicológica de la paciente requirió desarrollar un plan de tratamiento ajustado a sus necesidades. Pacientes susceptibles deben ser instruidos sobre la importancia de tener prácticas adecuadas de higiene oral y ameritan ser incluidos en programas de mantenimiento periodontal.
Background: Gingival enlargement induced by the use of drugs is a frequent clinical condition in patients who take anticonvulsants, immunosuppressive agents and calcium channel blockers. The gingival enlargement prevalence, as induced by drug use, is from 3% to 20% in the group with inflammatory gingival conditions. All these drugs cause clinical lesions and histological characteristics indistinguishable from one another, which eventually affect the function and aesthetics of the patients. Objective: To describe a comprehensive therapeutic management and the 12-month following in a patient with gingival enlargement induced by the use of tacrolimus and amlodipine. Case Description: A 22 year-old woman with Borderline Personality Disorder who also underwent a kidney transplant was referred to the dental service in the Hospital Infantil Universitario de San José (Bogotá, Colombia) due to gingival enlargement. The clinical examination showed an O'Leary plaque index of 84.3%, extended inflammation and gingival pockets about 4-6 mm. The kidney transplant team checked the periodontal treatment protocol that included: partnering with the family as a support network, design of a customized oral hygiene program, gingivectomy and regular periodontal maintenance. This therapeutic strategy allowed to reduce the plaque index and resulted in a favorable clinical condition. Conclusion: The systemic and psychological status of the patient required to design a treatment plan customized to her needs. Susceptible patients should be educated on how important it is to follow the appropriate oral hygiene practices and are eligible for periodontal maintenance programs.
Subject(s)
Kidney Transplantation/methods , Amlodipine/adverse effects , Gingival Diseases/chemically inducedABSTRACT
PURPOSE: Tacrolimus (FK506) is a new potent immunosuppressive agent which has been used as a primary immunosuppressive agent and rescue therapy for refractory rejection in kidney transplantation. In vitro, on a molecular basis, tacrolimus is 10 to 100 times more potent than cyclosporine. Complications associated with tacrolimus are similar to those seen in cyclosporine, including nephrotoxicity. An early marker of tacrolimus-induced nephropathy is tubular vacuolization, whereas long-term administration of tacrolimus is associated with striped interstitial fibrosis and arteriolar hyalinosis. However, morphological changes and pathogenesis of fibrosis in chronic tacrolimus-induced nephropathy remain poorly understood. Transforming growth factor (TGF)-beta1 has been implicated in the fibrosis of a number of chronic diseases of the kidney and other organs. This study was designed to clarify the ultrastructural changes of tacrolimus-induced nephropathy, and to evaluate the relationship between tacrolimus- induced nephropathy and expression of TGF-beta1. METHODS: Male ICR mice received tacrolimus daily at a dose of 2.5 mg/kg by intraperitoneal route for 12 weeks and sacrified 1, 4, 8, 10, and 12 weeks after the initiation of the study, respectively. The kidneys were removed, the cortex is carefully dissected from the medulla, and the tissues are processed for evaluation by light microscopy, electron microscopy, immunohistochemistry and RT-PCR for RNA analysis. RESULTS: Characteristic histological changes of tacrolimus-induced nephropathy were peritubular capillary and intraglomerular capillary congestions, vacuolizations of the tubular epithelium, pericapillary focal fibrosis, and tubular atrophy. Tacrolimus- treated kidneys had a progressive increase in the expression of TGF-beta1, especially in the glomerular and interstitial capillary endothelial cells and atrophied tubular epithelial cells. TGF-beta1 mRNA is expressed persistently in tacrolimus- treated mice for 12 weeks. CONCLUSION: It can be concluded that TGF-beta1 may be involved in the fibrogenesis in the tacrolimus-induced nephropathy.