Periodontitis and bone metabolism in patients with advanced heart failure and after heart transplantation

Abstract

Aims Heart failure (HF) is a multiorgan, pro-inflammatory syndrome that impairs bone metabolism. Pro-inflammatory cytokines and bone catabolism enhance periodontal disease, a local inflammatory, bacteria-induced disease that causes bone loss and periodontal soft tissue destruction. Methods and resultsMedical and dental examinations were performed on patients with HF (n = 39), following heart transplantation (post-HTx, n = 38) and controls (n = 32). Blood, saliva, and gingival crevicular fluid were analysed for bone metabolism and inflammation markers. HF average New York Heart Association classification was III. Average time since HTx was 1414 days. Pro-inflammatory tumour necrosis factor-alpha was higher in HF and HTx as compared with controls (P < 0.05). Both HF and HTx participants had higher levels of bone resorption marker C-terminal telopeptide and parathyroid hormone with subjects in the HF group having the highest serum levels of all groups (P ≤ 0.05). In contrast, 25-hydroxyvitamin D was lowest in HF. HF patients had greater clinical attachment loss, cumulative pockets depth (greater than 3 mm) and probing depth (P < 0.05) as compared with controls. Cumulative pockets depth correlated significantly with measures of the inflammatory burden, β-glucuronidase in saliva (r = 0.4863, P < 0.01), interleukin-1b in saliva (r = 0.5149, P < 0.01), and gingival crevicular fluid (r = 0.6056, P < 0.001) in HF. However, adjustment of periodontal results for measures of oral hygiene (plaque, bleeding on probing), systemic 25-hydroxyvitamin D, and race attenuated significant differences between groups.Conclusions Patients with HF exhibit more severe periodontal disease associated with increased bone turnover markers when compared with control patients. However, local and systemic factors may account for this association and should be evaluated in future studies.

Associations between tooth loss and prognostic biomarkers and the risk for cardiovascular events in patients with stable coronary heart disease

“…However, the observed differences were attenuated to non-significance after adjustment for markers of oral hygiene, race and 25-hydroxyvitamin D levels [29]. Overall, data on the role of PD in the pathophysiology of heart failure is largely lacking but the results from our present study and other studies are interesting from a hypothesis generating perspective and should be explored further.…”

“…All biomarkers were analyzed on a log-transformed scale using linear models. Geometric mean ratios are presented with 95% confidence intervals (CI) with the lowest tooth loss level (26)(27)(28)(29)(30)(31)(32) replacing significant renal dysfunction) [16], hemoglobin, white blood cells, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides. Cox proportional hazards models were used to calculate hazard ratios for MACE, CV death and stroke in relation to tooth loss levels, adjusting for biomarkers in addition to a previously reported multivariable model [4], co-variables of which are also listed in Table 3.…”

Autoantibodies against M5-muscarinic and beta1-adrenergic receptors in periodontitis patients

“…In the next step, we addressed the link between periodontitis, cardiac injury and generalized inflammation suggested by various studies, e.g. [ 24 ]. For that purpose, we measured the serum-levels of cardiac (proBNP, TpI) and inflammatory markers (CRP, IL-6) and compared these values between healthy individuals and periodontitis patients in pre-therapy samples.…”

Periodontal-induced chronic inflammation triggers macrophage secretion of Ccl12 to inhibit fibroblast-mediated cardiac wound healing

“…Periodontal disease (PD) is associated with adverse wound healing in response to injury across organ systems, including poor cardiac responses to myocardial infarction (MI) (1)(2)(3)(4)(5)(6). MI incidence correlates with the number of pockets > 4 mm deep, bleeding sites after probing, and severity of tooth loss, even after adjustment for known cardiovascular risk factors (e.g., smoking, diabetes, or hypertension) (4).…”

“…MI incidence correlates with the number of pockets > 4 mm deep, bleeding sites after probing, and severity of tooth loss, even after adjustment for known cardiovascular risk factors (e.g., smoking, diabetes, or hypertension) (4). Antibodies against the periodontal pathogen Porphyromonas gingivalis are also elevated in MI patients (4), and heart-failure patients exhibit increased bone turnover markers in circulation and a more advanced PD phenotype compared with healthy control patients (6). In addition, severe periodontitis is more prevalent among post-MI heart-failure patients than dilated cardiomyopathy-induced heart-failure patients (5).…”