RESUMEN
AIM: To evaluate the impact of two non-surgical periodontal treatment modalities on metabolic and periodontal clinical parameters in subjects with type 2 diabetes mellitus (T2DM) and poor glycaemic control and chronic periodontitis. MATERIAL AND METHODS: A randomized controlled clinical trial was conducted. Ninety-three T2DM subjects with glycosylated haemoglobin (HbA1c) > 7% were randomly assigned to one of two groups receiving scaling with root planing in multiple sessions quadrant-by-quadrant (Q by Q) or within 24 hr (one stage). Periodontal parameters, HbA1c, glycaemia blood levels (FPG) and C-reactive protein (CRP) values were assessed at baseline and at 3 and 6 months post-therapy. RESULTS: At 6 months, HbA1c had decreased by 0.48% in the Q by Q group and by 0.18% in the one-stage group (p = 0.455). After therapy, subjects with an initial HbA1c < 9% showed an increase of 0.31% (p = 0.145), compared with a decrease of 0.88% (p = 0.006) in those with an initial HbA1c ≥ 9%. Periodontal parameters improved significantly (p < 0.0001) post-therapy, with similar results for both treatment modalities. CONCLUSION: Periodontal therapy had the greatest impact on HbA1c reduction on patients with an HbA1c > 9% regardless of treatment modality. Both modalities resulted in significant improvements in periodontal parameters.
Asunto(s)
Periodontitis Crónica , Diabetes Mellitus Tipo 2 , Raspado Dental , Hemoglobina Glucada , Humanos , Aplanamiento de la RaízRESUMEN
Background: Sodium and potassium ions are involved in the regulation of blood pressure and the genesis of hypertension. Aim: to assess internal potassium balance, as a measure of sodium pump activity, in subjects with essential hypertension and diabetic patients. Patients and methods: Eleven hypertensive subject, 5 non-insulindependent diabetics and 16 age matched controls were studied. An acute oral load of 0.8 mEq/Kg body weight of KCI was administered and blood samples were drawn every 30 min thereafter, until 120 min, to measure plasma K+ levels. Urinary K+ excretion during this period was also measured. In eight hypertensive patients, the test was repeated after two week of supplentation with 60 mEq/day of KCI. The maximal increase in plasma potassium levels and the time required to achieve the maximum concentration was recorded. Results: All patients had normal serum creatinine levels. Mean fasting blood glucose of diabetic patients was 133 ñ 15.1 mg/dl. No difference between patients and controls in maximal increase plasma potassium increase, was observed. In hypertensive patients the lapse to achieve the maximal potassium concentration was longer than in controls. After the period of potassium supplementation in hypertensive patients, tbere was a significant increase in basal plasma K+ levels and the temporal pattern of plasma potassium increase was similar to that of controls. Between 63 and 68 percent of retained K+ load was translocated to the intracellular space at 120 min in all study groups. Conclusions: Internal potassium balance is not significantly altered in subjects with essential hypertension or in non-insulin-dependent diabetics