Protective effect of alpha‐lipoic acid against apical periodontitis‐induced cardiac injury in rats

Abstract

This study was designed to assess the possible protective effect of alpha‐lipoic acid (ALA) on apical periodontitis (AP)‐induced cardiac injury. Wistar albino rats were randomized into four groups: control; ALA; AP; and ALA + AP. Rats of the control and ALA groups were not endodontically treated, but saline and ALA (100 mg kg−1) were administered. In rats of the AP and ALA + AP groups, the pulp chambers of mandibular first molar teeth were exposed and left open for 30 d to induce AP. Saline and ALA (100 mg kg−1) were administered intraperitoneally every 24 h during the experiment. At the end of the experiment, the rats were killed. Establishment of AP was verified by radiographic and histopathological evaluation. Serum alkaline phosphatase (ALP), lactate dehydrogenase (LDH), creatine kinase (CK), and superoxide dismutase (SOD) activities were determined using an automated biochemical analyzer, and the structural cardiac injury was assessed pathologically. Serum ALP, LDH, and CK activities were elevated, and SOD activities were decreased, in the AP group. The changed enzyme activities were significantly normalized by treatment with ALA. We conclude that ALA administration alleviated the AP‐induced heart injury and improved cardiac structure and function, and therefore this agent may be of potential therapeutic value in protecting cardiac tissue from systemic injury caused by AP.

Cardiac, biochemical and histopathological analysis reveals impaired heart function in hypertensive rats with apical periodontitis

“…According to literature data, there have been no studies that examined the pathohistological changes of the heart under the influence of AP in spontaneously hypertensive conditions; therefore, it could only be compared with the results of studies that investigated the effect of AP on the heart in normotensive conditions. The results of this study partially coincide with the study investigated by Sehirli et al (2019), which showed that AP in normotensive conditions caused oedema, regions of myocardial congestion and the influx of inflammatory cells.…”

“…Regarding the components of the antioxidant defence system, myocardial SOD activity was lower in SHR + AP and AP groups compared to their control groups, whilst the level of CAT and GSH was similar between groups. The experimental study of Sehirli et al (2019) which dealt with assessing the possible protective effect of alpha‐lipoic acid on AP induced cardiac injury, showed that serum SOD activities were decreased in the AP group compared with the apically healthy control group, as in the present study with myocardial SOD activity. These results suggest the importance of deficiency of antioxidant enzymes in cardiac damage that has developed as a result of AP.…”

“…In contrast to spontaneous hypertensive conditions, AP led to the appearance of the most prominent changes in the myocardium, such as zonal necrosis of a large number of muscle cells with fibre fragmentation, nucleus loss and cytoplasmic hypereosinophilia. It is believed that the possible cause of these changes in the heart is the systemic growth of bacteria or the spread of immune complexes at a distance (Sehirli et al, 2019; Zhang et al, 2016). According to literature data, there have been no studies that examined the pathohistological changes of the heart under the influence of AP in spontaneously hypertensive conditions; therefore, it could only be compared with the results of studies that investigated the effect of AP on the heart in normotensive conditions.…”

“…The patency of the root canals’ was explored using a size 8 K‐file (Dentsply Sirona). The pulp chambers remained open to the oral environment for 4 weeks to allow the creation of apical lesions (Sehirli et al, 2019).…”

“…Additionally, the association between endodontic conditions and CVDs could be attributed to the fact that both share common risk factors or depend on the same genetic polymorphisms (Jiménez‐Sánchez et al, 2020). Experimental studies have reported that AP is related to a rise in the activity of lactate dehydrogenase, creatine kinase and alkaline phosphatase, as well as reduced activity of superoxide dismutase in heart tissue (Sehirli et al, 2019). Also, AP has been reported to be associated with increased production of reactive species in the heart and decreased catalase activity and vitamin C levels in the rat heart and pancreas (Barcelos et al, 2020).…”