Anti-Infection of Oral Microorganisms from Herbal Medicine of Piper crocatum Ruiz & Pav

Abstract

The WHO Global Status Report on Oral Health 2022 reveals that oral diseases caused by infection with oral pathogenic microorganisms affect nearly 3.5 billion people worldwide. Oral health problems are caused by the presence of S. mutans, S. sanguinis, E. faecalis and C. albicans in the oral cavity. Synthetic anti-infective drugs have been widely used to treat oral infections, but have been reported to cause side effects and resistance. Various strategies have been implemented to overcome this problem. Synthetic anti-infective drugs have been widely used to treat oral infections, but they have been reported to cause side effects and resistance. Therefore, it is important to look for safe anti-infective alternatives. Ethnobotanical and ethnopharmacological studies suggest that Red Betel leaf (Piper crocatum Ruiz & Pav) could be a potential source of oral anti-infectives. This review aims to discuss the pathogenesis mechanism of several microorganisms that play an important role in causing health problems, the mechanism of action of synthetic oral anti-infective drugs in inhibiting microbial growth in the oral cavity, and the potential of red betel leaf (Piper crocatum Ruiz & Pav) as an herbal oral anti-infective drug. This study emphasises the importance of researching natural components as an alternative treatment for oral infections that is more effective and can meet global needs.

Keywords: Piper crocatum; anti-infection; antibacterial; antifungal; oral pathogen.

Figure 1

Structure of an antifungal compound with a mechanism of systemic infection Amphotericin B (1), Flucytosine (2), Ketoconazole (3), Fluconazole (4), Miconazole (5), and Hydroxystilbamidine (6).

Figure 2

Structure of an antifungal compound with a mechanism of systemic infection: Griseofulvin (7), Clotrimazole (8), Econazole (9), Isoconazole (10), Tioconazole (11), Bifonazole (12), Nystatin (13), and Tolnaftate (14).

Figure 3

Structure of an antifungal compound with a mechanism of dermatophyte and mucocutaneous infections: Candicidin (15), Undecylenic acid (16), and Natamycin (17).

Figure 4

Summarized synthesis of ergosterol, the fungal sterol, and detailed steps of CYP51 conversion of lanosterol to 14α-demethyl lanosterol.

Figure 5

Mechanism of inhibition by antifungal echinocandins by inhibiting the synthesis of beta-1,3 glucan synthase.

Figure 6

Red Betel leaves.

Figure 7

Structure of the compound β-Sitosterol (18), 2 -(5’),6’-dimethoxy-3’, 4’-methylenedioxyphenyl)-6-(3’,4’,5 trimethoxyphenyl)-dioxabiclo [3,3,0] octane (19). Structure of (1’R, 2’R, 3’S, 7S, 8R)-Δ5’,8’-2’-acetoxy-3,4,5,3’, 5’-pentamethoxy-4’-oxo-8’.1,7.3-neolignan (20) and (1’R, 2’R, 3’S, 7S, 8R)-Δ5’, 8’-2’-hydroxy-3, 4, 5, 3’, 5’-pentamethoxy-4’-oxo-8.1’, 7.3’-neolignan (21).

Figure 8

Structure of the compound β-phenylethyl β-D-glucoside (22), Benzyl-β-D-glucoside (23), hydroxytyrosol-1glucopyranoside (24), Gentisic acid (25), Loliolide (26), (6S,9S)-roseoside (27), Vitexin 2″-O-rhamnoside (28), and structure of Pipcroside A (29), Pipcroside B (30), Pipcroside C (31), Crocatin B (32).

Figure 9

Structure of antifungal constituents of P. crocatum, Piperyamide A (33), Piperyamine A (34), and Stigmasterol (35).

Figure 10

Structure of the compound camphene (36), sabinene (37), caryophyllene (38), α-Humulen (39), Mirsen (40).

Figure 11

Biofilm formation by Candida albicans.

Figure 12

Pathogenic mechanism of cross-kingdom interaction between C. albicans and oral bacteria.