Systemic acute‐phase reactants, C‐reactive protein and haptoglobin, in adult periodontitis

Systemic acute‐phase reactants, C‐reactive protein and haptoglobin, in adult periodontitis Capture ELISAs with biotinylated monospecific antibodies were developed to detect both C‐reactive protein (CRP) and haptoglobin (Hp) in serum of adult periodontitis (AP) patients and normal subjects. Each acute‐phase reactant was significantly increased in serum from AP patients with CRP at 9.12 ±1.61 mg/l versus 2.17 ± 0.41 mg/l (P < 0.001) and Hp at 3.68 ± 0.37 g/l versus 1.12 ± 0.78 g/l (P < 0.001). Assessment of clinical characteristics of the patients' periodontal disease indicated that CRP and Hp levels were significantly increased in patients with the most frequent disease active episodes (P < 0.02 and P < 0.001, respectively). Longitudinal examination of the Hp levels showed a significant decrease following scaling and root planing (3.68 versus 2.38 g/l; P < 0.01). After a 2‐year administration of 50 mg/b.i.d. Flurbiprofen (a non‐steroidal anti‐inflammatory drug), significantly decreased Hp levels were noted (P < 0.005). CRP levels declined by 35–40% after 1–2 years of treatment with the drug (P < 0.05). The findings indicated that localized infections resulting in increased inflammation and tissue loss in the periodontium elicit systemic host changes manifest by increases in two acute‐phase reactants. The conclusions are that either these molecules are formed locally and distributed to the serum, or these presumably localized infections impact upon the systemic components of the host protective responses. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical & Experimental Immunology Wiley

Systemic acute‐phase reactants, C‐reactive protein and haptoglobin, in adult periodontitis

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Abstract

Capture ELISAs with biotinylated monospecific antibodies were developed to detect both C‐reactive protein (CRP) and haptoglobin (Hp) in serum of adult periodontitis (AP) patients and normal subjects. Each acute‐phase reactant was significantly increased in serum from AP patients with CRP at 9.12 ±1.61 mg/l versus 2.17 ± 0.41 mg/l (P < 0.001) and Hp at 3.68 ± 0.37 g/l versus 1.12 ± 0.78 g/l (P < 0.001). Assessment of clinical characteristics of the patients' periodontal disease indicated that CRP and Hp levels were significantly increased in patients with the most frequent disease active episodes (P < 0.02 and P < 0.001, respectively). Longitudinal examination of the Hp levels showed a significant decrease following scaling and root planing (3.68 versus 2.38 g/l; P < 0.01). After a 2‐year administration of 50 mg/b.i.d. Flurbiprofen (a non‐steroidal anti‐inflammatory drug), significantly decreased Hp levels were noted (P < 0.005). CRP levels declined by 35–40% after 1–2 years of treatment with the drug (P < 0.05). The findings indicated that localized infections resulting in increased inflammation and tissue loss in the periodontium elicit systemic host changes manifest by increases in two acute‐phase reactants. The conclusions are that either these molecules are formed locally and distributed to the serum, or these presumably localized infections impact upon the systemic components of the host protective responses.

Journal

Clinical & Experimental ImmunologyWiley

Published: Feb 1, 1997

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