**1. Introduction**

Periodontal diseases are a group of inflammatory conditions affecting the connective tissues surrounding teeth. Periodontitis, a specific type of periodontal disease, is a major cause of tooth loss and the prevalence of its moderate to severe forms in adult Western populations is approximately 50% [1,2]. Periodontitis is caused by gram-negative bacteria which induce a host inflammatory response, resulting in the destruction of tissues that supports the teeth and also has adverse systemic effects [3].

Type 2 diabetes mellitus (type 2 DM) is a metabolic disorder ranging from insulin resistance to insulin deficiency, with poor glycaemic control presenting as a predominant feature [3]. Diabetes is also a major risk factor for periodontitis, and the risk of developing periodontitis is increased approximately three times in patients with diabetes compared with non-diabetic individuals [4]. There is an increasing prevalence of type 2 DM worldwide, and this is expected to contribute to an increase in diabetes-related complications [5].

Cardiovascular disease (CVD) is also one of the major complications associated with diabetes, and there is a high prevalence of cardiovascular risk factors and markers of cardiovascular organ injury in patients with type 2 DM. Ninety-seven percent of patients with diabetes are dyslipidaemic, with a

characteristic pattern of increased plasma triglycerides and decreased high density lipoprotein (HDL) cholesterol. In a large clinical study with an average follow-up period of 3.9 years, low density lipoprotein (LDL) cholesterol, non-HDL cholesterol, apolipoprotein B, triglyceride, and homocysteine levels all increased over time, with most participants also having low HDL levels [6]. The downregulation of the enzyme lipoprotein lipase due to low insulin levels may be the cause of the dyslipidaemic profiles noted in diabetic individuals [7]. Other mechanisms involved linking diabetes to higher CVD risk involve chronic oxidative stress in diabetics, purportedly related to the metabolism of excess substrates (glucose and fatty acids [8]) and a state of chronic, low-level inflammation [9] in diabetes.

Recent intervention trials have demonstrated that anti-inflammatory periodontitis therapy may reduce serum levels of glycated haemoglobin (HbA1c) and high sensitivity C-reactive protein (hsCRP) [10–16], demonstrating the capacity to modulate glucose control and cardiovascular risk. However, little attention has been paid to the potential e ffects of periodontitis therapy in patients with diabetes to improve lipid profiles. This systematic review aims to evaluate the scientific evidence of the impact of periodontal therapy on lipid profiles in patients with type 2 DM.
