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Review
. 2023 May 11;11(5):1269.
doi: 10.3390/microorganisms11051269.

Green Alternatives as Antimicrobial Agents in Mitigating Periodontal Diseases: A Narrative Review

Seyed Ali Mosaddad  1 , Ahmed Hussain  2 , Hamid Tebyaniyan  3
Affiliations
Review

Green Alternatives as Antimicrobial Agents in Mitigating Periodontal Diseases: A Narrative Review

Seyed Ali Mosaddad et al. Microorganisms. .

Abstract

Periodontal diseases and dental caries are the most common infectious oral diseases impacting oral health globally. Oral cavity health is crucial for enhancing life quality since it serves as the entranceway to general health. The oral microbiome and oral infectious diseases are strongly correlated. Gram-negative anaerobic bacteria have been associated with periodontal diseases. Due to the shortcomings of several antimicrobial medications frequently applied in dentistry, the lack of resources in developing countries, the prevalence of oral inflammatory conditions, and the rise in bacterial antibiotic resistance, there is a need for reliable, efficient, and affordable alternative solutions for the prevention and treatment of periodontal diseases. Several accessible chemical agents can alter the oral microbiota, although these substances also have unfavorable symptoms such as vomiting, diarrhea, and tooth discoloration. Natural phytochemicals generated from plants that have historically been used as medicines are categorized as prospective alternatives due to the ongoing quest for substitute products. This review concentrated on phytochemicals or herbal extracts that impact periodontal diseases by decreasing the formation of dental biofilms and plaques, preventing the proliferation of oral pathogens, and inhibiting bacterial adhesion to surfaces. Investigations examining the effectiveness and safety of plant-based medicines have also been presented, including those conducted over the past decade.

Keywords: anti-infective agents; herbal medicine; periodontal diseases; plant extracts; plants.

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Conflict of interest statement

The authors declare that they have no competing interest.

Figures

Figure 1
Figure 1
Microbial complexes involved in the progression and development of periodontal diseases [14].
Figure 2
Figure 2
Personal, social, systemic, and local risk factors associated with oral dysbiosis lead to periodontal disease development and progression through activating pathogenic pathways [19].
Figure 3
Figure 3
An overview of how the mentioned T and B cells can affect periodontal health. Treg and CD8+ T cells produce IL-10 and TGF-β to maintain periodontal health. To maintain periodontal health, T cells produce amphiregulin and IL-17. Antibodies produced by B cells limit periodontal inflammation. Pro-inflammatory cytokines are released by activated Th1, Th2, and Th17 cells during periodontal disease. A combination of T and B cells produce RANKL, which activates osteoclasts. By clonally activating B cells, Tfh cells can cause local tissue destruction by producing autoantibodies against collagen, fibronectin, and laminin. A lack of Tregs or impaired function probably causes periodontitis. Other cells can also activate osteoclasts by producing IL-17 [45].
Figure 4
Figure 4
Different mechanisms of action through which garlic extract’s compounds assert antibacterial, antifungal, and antiviral effects [78].
Figure 5
Figure 5
The main phenolic compounds of the Aloe vera plant and their chemical structures [102].
Figure 6
Figure 6
Results of a study on beneficial anti-inflammatory effects of Aloe vera + scaling treatment [(a) baseline; (b) one-month post-op; and (c) three-month post-op] to reduce plaque-induced gingivitis [103].
Figure 7
Figure 7
The botanical source of turmeric (A). Powdered curcumin (B). Curcumin in enol and keto forms (C) [235].
Figure 8
Figure 8
Live/dead bacLight® fluorescent microscopy images. Avital fluoresces are in red, while vital bacteria are in green. (A) NaCl treatment as negative control, (B) CHX treatment as positive control, and (C) DMSO treatment as toxicity control, I. viscosa groups in concentrations: 10 mg/mL (D) and 30 mg/mL (E) [283].
Figure 9
Figure 9
An evaluation of manuka honey’s bactericidal effect (a) and effective manuka honey incubation period (b) [357].
Figure 10
Figure 10
Different concentrations of Tulsi on growth inhibition of P. gingivalis (a); 5% Tulsi against A.a (b); 10% Tulsi against A. a (c); and against P. intermedia (d) [314].
Figure 11
Figure 11
Anti-inflammatory, oxidative stress, cytotoxicity, and antimicrobial characteristics of using Pistacia lentiscus essential oils against periodontal bacteria and Candida albicans (GK: gingival keratinocytes, PDLF: periodontal ligament fibroblasts; GF: gingival fibroblasts; and DOK: dysplastic oral keratinocytes) [414].
Figure 12
Figure 12
A histological section of a rat incisor tooth and its surrounding periodontal tissues. Treatment control group (A): mild inflammatory cells (black arrows) with intact junctional epithelium and a stable bony surface with dense, well-formed bone and multiple blood vessels (red arrows) (H&E, scale bar 10 μm in section (a), and 20 μm in section (b,c)). Testing group (B): mild inflammatory cells (black arrowheads) with intact junctional epithelium and well-formed, dense bone (H&E, scale bar 10 μm in section (a), and 20 μm in section (b–d)) (AB; alveolar bone, PL; periodontal ligament and C; cementum) [415].
Figure 13
Figure 13
The chemotherapeutic effects of Salvadora persica on periodontal diseases [517].
Figure 14
Figure 14
A comparison of the effect of Terminalia chebula ethanolic extract and ampicillin (Amp) on the growth of A. a, S. mutans, and other dental plaque bacteria (DPB#1, DPB#2, and DPB#3) [321].
Figure 15
Figure 15
An illustration of flavan-3-ols and proanthocyanidin immunomodulatory activities in periodontitis [550].
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