# The Potential of Cannabidiol in the Management of Oral Infections
## 2 Chemical and Pharmacological Aspects of Cannabidiol  
CBD, whose chemical structure is represented in Figure 2, is a major non-psychoactive phytocannabinoid derived from the plant _Cannabis sativa_ L. First isolated in 1940, CBD has garnered increasing scientific attention for its wide-ranging therapeutic properties, including anti-inflammatory, analgesic, anxiolytic, antioxidant, and antimicrobial effects. Unlike delta-9-tetrahydrocannabinol (THC), the principal psychoactive component of cannabis, CBD does not induce intoxication and has a favorable safety profile, making it a promising candidate for various clinical applications [27]. CBD is a terpenophenolic compound with the molecular formula C\({}_{21}\)H\({}_{30}\)O\({}_{2}\) and a molecular weight of 314.46 g/mol. Structurally, it is a bicyclic compound featuring a resorcinol moiety and a pentyl side chain. In the cannabis plant, CBD is synthesized from cannabinoid acid (CBGA) through the action of CBD synthase, resulting in cannabidiolic acid (CBDA), which is subsequently decarboxylated to CBD via heat or light exposure. CBD exerts its biological effects through complex interactions with multiple molecular targets, as follows: (i) Cannabinoid Receptors: CBD has low affinity for the classical cannabinoid receptors CB1 and CB2, but modulates their activity indirectly. It acts as a negative allosteric modulator of CB1, potentially reducing the psychoactive effects of THC, and may exert partial agonistic or antagonistic actions at CB2. (ii) Transient Receptor Potential (TRP) Channels: CBD activates the TRPV1, TRPV2, and TRPA1 channels, which are involved in pain perception, inflammation, and thermoregulation. (iii) Serotonin Receptors: it acts as a partial agonist at the 5-HT1A receptor, contributing to its anxiolytic and neuroprotective properties. (iv) PPAR\(\gamma\) Activation: CBD activates peroxisome proliferatorator-activated receptor gamma (PPAR\(\gamma\)), influencing inflammatory and metabolic pathways. (v) Adenosine Signaling: CBD inhibits adenosine reuptake, leading to increased adenosine signaling and associated anti-inflammatory and cardioprotective effects [27]. CBD displays broad-spectrum antimicrobial activity, particularly against Gram-positive bacteria, and has shown efficacy in disrupting biofilms, which are a major virulence factor in many oral and systemic infections [24; 28]. The lipophilic structure of CBD enables its integration into microbial membranes, where it causes structural disruption and increased membrane permeability (membrane disruption). This leads to the leakage of cellular contents, impaired membrane potential, and ultimately, cell death. Electron microscopy studies have revealed morphological damage in bacterial membranes treated with CBD, supporting this mechanism [29]. Figure 2: Chemical structure of CBD. Biofilms are dense microbial communities that confer resistance to antibiotics and host defenses. CBD has been shown to inhibit biofilm formation and reduce established biofilms, particularly in oral pathogens such as _Streptococcus mutans_ and _Enterococcus faecalis_. This anti-biofilm effect may be attributed to CBD's interference with quorum sensing pathways and extracellular polymeric substance (EPS) production [19; 24; 28]. CBD has been shown to enhance the efficacy of conventional clinical antibiotics in some settings, potentially through synergistic interactions that facilitate greater microbial susceptibility. For example, CBD has been reported to potentiate the effects of antibiotics like bactircin and erythromycincin, possibly by facilitating antibiotic entry into bacterial cells or by disrupting resistance mechanisms [30]. CBD also exhibits antifungal activity, although this has been less extensively studied against _Candida albicans_ and related species, likely via similar membrane-disruptive mechanisms [24]. Some evidence suggests antiviral effects, although these remain to be fully elucidated in oral contexts [31].