Abstract
AimThe aim of the study is to assess the long-term effect of active periodontal therapy on serum inflammatory parameters in patients with aggressive (AgP) and chronic (ChP) periodontitis in a non-randomised clinical study.MethodsTwenty-five ChP and 17 AgP were examined clinically prior to (baseline), 12 weeks and 60 months after subgingival debridement of all pockets within 2 days. Systemic antibiotics were prescribed if Aggregatibacter actinomycetemcomitans was detected (10 AgP, 8 ChP), flap surgery was rendered if required. Neutrophil elastase (NE), C-reactive protein (CRP), lipopolysaccharide binding protein, interleukin 6, 8, and leukocyte counts were assessed at baseline, 12 weeks and 60 months.ResultsClinical parameters improved significantly in both groups from 12 weeks to 60 months. Eleven AgP and 18 ChP patients received surgical treatment after the 12 weeks examination. Only 3 patients in each group attended ≥ 2 supportive maintenance visits per year. NE and CRP were significantly higher in AgP than ChP at baseline and 60 months (p < 0.01). For leukocyte counts in ChP, significant changes were observed (baseline: 6.11 ± 1.44 nl−1; 12 weeks: 5.34 ± 1.40 nl−1; 60 months: 7.73 ± 2.89 nl−1; p < 0.05). Multiple regression analysis identified African origin, surgical treatment and female sex to correlate with better clinical improvement.ConclusionDespite comprehensive periodontal treatment, AgP patients exhibit higher NE and CRP levels than ChP patients up to 5 years after therapy.Clinical relevanceSystemic inflammatory burden in AgP patients is higher than in ChP patients even 5 years after periodontal treatment.
Highlights
Even everyday practices such as tooth brushing, flossing, and chewing result in frequent bacteraemia in individuals suffering from untreated periodontal disease [1]
Frequent bacteraemia and systemic spread of proinflammatory cytokines [2] from periodontal pockets cause the release of neutrophil elastase (NE) and acute phase proteins (e.g. C-reactive protein: CRP)
Increased serum NE and CRP caused by periodontitis may link periodontal and systemic diseases [cardiovascular disease (CVD), ischemic stroke [6,7,8], as well as chronic obstructive pulmonary diseases (COPD) [9, 10]]
Summary
Even everyday practices such as tooth brushing, flossing, and chewing result in frequent bacteraemia in individuals suffering from untreated periodontal disease [1]. Frequent bacteraemia and systemic spread of proinflammatory cytokines [2] from periodontal pockets cause the release of neutrophil elastase (NE) and acute phase proteins (e.g. C-reactive protein: CRP). Serum CRP [3] and NE [4, 5] are elevated in patients with untreated periodontitis compared to healthy controls. Increased serum NE and CRP caused by periodontitis may link periodontal and systemic diseases [cardiovascular disease (CVD), ischemic stroke [6,7,8], as well as chronic obstructive pulmonary diseases (COPD) [9, 10]]. A recent study compared NE and CRP levels in patients suffering from a similar severity of untreated aggressive and chronic periodontitis. NE and CRP levels in aggressive periodontitis were found to be elevated compared to chronic
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