Hyperlipidemia is necessary for the initiation and progression of atherosclerosis by severe periodontitis in mice

• Published in: Molecular medicine reports Vol. 26; no. 2
• Main Authors: Suh, Jin Sook, Kim, Sharon Y.J, Lee, Sung Hee, Kim, Reuben H, Park, No-Hee
• Format: Journal Article
• Language: English
• Published: Athens Spandidos Publications 01.08.2022; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Alveolar bone; Alzheimer's disease; Apolipoprotein E; Arteriosclerosis; Atherosclerosis; Bone loss; Care and treatment; Cholesterol; Complications and side effects; Coronary vessels; Cytokines; Development and progression; Diagnosis; Ethanol; Gene expression; General anesthesia; Gum disease; Hyperlipidemia; Inflammation; Inflammatory diseases; Laboratory animals; Osteoclasts; Periodontitis; Phosphatase; Psoriasis; Reverse transcription; Rheumatoid arthritis; Risk factors; Scleroderma; Systemic diseases; Systemic lupus erythematosus; Systemic sclerosis; United States; Los Angeles California; United States > US; California
• ISSN: 1791-2997; 1791-3004
• DOI: 10.3892/mmr.2022.12789

Hyperlipidemia is a major risk of atherosclerosis; however, systemic inflammatory diseases such as rheumatoid arthritis, psoriasis, systemic lupus erythematosus and systemic sclerosis are also known risks for the development of atherosclerosis. Periodontitis, a local and systemic inflammatory condition, has also been reported as a risk for atherosclerosis, but the specific link between periodontitis and atherosclerosis remains somewhat controversial. We previously reported that ligature-induced periodontitis exacerbates atherosclerosis in hyperlipidemic Apolipoprotein E-deficient ([ApoE.sup.-/-]) mice. To understand whether hyperlipidemia is necessary for the development and exacerbation of atherosclerosis associated with periodontitis, the present study created ligature-induced periodontitis in both wild-type (WT) and [ApoE.sup.-/-] mice. Subsequently, the status of local, systemic and vascular inflammation, serum lipid contents and arterial lipid deposition were examined with histological analysis, [mu]CT, enface analysis, serum lipid and cytokine measurements, reverse transcription-quantitative PCR and immunohistochemical analysis. Ligature placement induced severe periodontitis in both WT and [ApoE.sup.-/-] mice at the local level as demonstrated by gingival inflammation, alveolar bone loss, increased osteoclastic activities and inflammation in alveolar bone. Systemic inflammation was also induced by ligature placement in both WT and [ApoE.sup.-/-] mice, albeit more so in [ApoE.sup.-/-] mice. The serum cholesterol levels were not altered by the ligature in both WT and [ApoE.sup.-/-] mice. However, the vascular inflammation and arterial lipid deposition were induced by ligature-induced periodontitis only in [ApoE.sup.-/-] mice, but not in WT mice. The present study indicated that the coupling of systemic inflammation and hyperlipidemia was necessary for the development and exacerbation of atherosclerosis induced by ligature-induced periodontitis in mice. Key words: atherosclerosis, hyperlipidemias, periodontitis, systemic inflammation