## 1 Introduction  
Approximately 500 million children suffer from tooth decay in their primary dentition, while Global Burden of Disease (2017) reports that untreated tooth decay in permanent teeth is the most common health condition [1]. Dental caries is a chronic infectious disease and the most common cause of pulpal pathology, such as pulp inflammation (or pulpitis) [2]. Dental pulp inflammation can occur before bacteria take over the pulp tissue. Bacteria and their metabolic products, such as lipoteichoic acid (LTA), can diffuse through dental tubules and may initiate the mechanisms of the immune response in the dental pulp [3]. Dental pulp is a loose connective tissue located in a low-compliance environment. Bacterial invasion is accompanied by macroscopic changes, such as vasodilitation and a decrease in the blood flow resistance [4]. Intravascular pressure and capillary blood flow increases, accompanied by leukocyte extravasation and an accumulation of serum proteins. These vascular alterations are followed by the recruitment of immune cells, which tend to eliminate the pathogens and their metabolites. If microbial irritation continues, exceeding the pulp's immune capacity, local hypoxia is installed by compression of the venules, metabolic waste products and CO2 increase, and further vasodilation occurs. All of these lead to the spreading of inflammation. Considering this, if the edema from inflammation is not resolved by removing the insult, tooth pain is the first and main sign of pulp pathology [3]. An initial invasion of microbes activates an innate immunity of the dentine/pulp complex. Innate immunity, as a response to caries, is provided by the action of odontoblasts; the effects of neuropeptides and neurogenic inflammation; an increased outflow of the dentinal fluid and intratabular deposition of immunoglobulins; the functioning of innate immune cells, such as immature and pulpal dendritic cells (DCs); monocytes and macrophages; lymphocytes, such as natural killer (NK) cells and T cells, and their cytokines and chemokines [5]. All of these components stop bacterial penetration and abolish the invading bacteria by recognizing them or their components [6]. Adapative immunity with cellular and specific antibody responses is activated when an innate response can't eliminate the pulp injury. The transition from innate to adaptive immunity is believed to take place in irreversibly inflamed pulp tissue, located at less than 2 mm from the deep carious lesion [6]. LTA is produced by cariogenic bacteria after fermenting sucrose, and is attached to the cell membranes of streptococci. LTA can initiate the innate immune system by binding to CD14, by activating the signaling with Toll-like receptors (TLRs), and by stimulating the release of the following cytokines from innate immune cells: tumor necrosis factor-alpha (TNF-\(\alpha\)), interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), interleukin-12 (IL-12), interleukin-18 (IL-18), and IFN-\(\gamma\)[3]. TNF-\(\alpha\) and IL-1 promote the expression of adhesion molecules, which induce extravasation of phagocytes during inflammation, while IFN-\(\gamma\), produced by NK cells, activates phagocytes and enhances TNF-\(\alpha\) actions on endothelial cells. Macrophages produce IL-10, which has a crucial role in the control of innate and cell-mediated immunity by inhibiting macrophages and DCs's functions. In response to bacteria or cytokines, various cell types, such as IL-1 and TNF-\(\alpha\), secrete IL-6, which intensifies the production of neutrophils and acute-phase proteins from bone marrow progenitors. IL-12 and IL-18 produced by resting T cells can direct the following adaptative cellular immune response [6]. Matrix metalloproteinases (MMPs) can degrade extracellular matrix (ECM) proteins and participate in tissue homeostasis [4,7].