Table 5.
Summary of the studies included according to the cannabinoids and periodontal lesions.
| Cannabinoids and Periodontal Lesions | |||||||||
|---|---|---|---|---|---|---|---|---|---|
| Authors | Drug | Study Design | Experimental Model | Administration Protocol | Results | Test | Control | Subjects/Specimens | Study Time |
| Kozono et al. [107] | Endocannabinoid | In vitro study/In vivo on rats | Periodontal fibroblasts/periodontal wound healing | Cell culture | Higher proliferation of human gingival fibroblasts (HGFs) by AEA, that can be reduced by AM251 and AM630, selective antagonists of CB1 and CB2 |
anandamide (AEA)/2-arachidonoylglycerol (2-AG) | anandamide (AEA)/2-arachidonoylglycerol (2-AG)+ AM251 and AM630, which are selective antagonists of CB1 and CB2, | 4 specimens | 0, 3 days, 7 days, 14 days |
| Thomson et al. [132] | Cannabis Smoking | Prospective cohort study | Periodontitis | Cannabis exposure | Cannabis smoking may be a risk factor for periodontal disease that is independent of the use of tobacco |
1: cannabis some exposure; 2: cannabis high exposure (182; 20.2%). | No exposure | 1037 subjects | 1 year |
| Shariff et al. [133] | cannabis (marijuana and hashish) | Cohort study | Periodontal examination | - | Cannabis use was related to with deeper probing depths, more clinical attachment loss and higher odds of having severe periodontitis. | Cannabis exposure | Non cannabis users | 1938 subjects | 1 year |
| Nogueira-Filho et al. [134] | Cannabinoids | In vivo on rats | Experimental periodontitis | Cannabis exposure | cannabis smoke may impact alveolar bone by increasing bone loss |
marijuana smoke inhalation | No exposure | 30 specimens | 30 days |
| Ossola et al. [135] | synthetic cannabinoid | In vitro study/In vivo on rats | Lipopolysaccharide-Induced Periodontitis | topical administration on gingival tissues | anti-inflammatory, osteoprotective and pro-homeostatic effects of HU-308 in oral tissues | 1: Vehicle; 2: HU-308 (500 ng/mL); 2: LPS/HU-308 (500 ng/mL) | No treatment | 24 specimens | 45 days |
| Napimoga et al. [137] | Cannabis Smoking | In vivo on rats | LPS Experimental periodontitis | Vein administration | Cannabidiol is related to a lower bone resorption by the inhibition of the RANK/RANKL expression | 1: vehicle; 2: Cannabidiol (CBD) | No treatment | 30 specimens | 30 days |
| Ossola et al. [136] | synthetic cannabinoid | In vitro study/In vivo on rats | Lipopolysaccharide-Induced Periodontitis | topical Meth-AEA (500 ng/mL) |
Beneficial effects of treatment with Meth-AEA on gingival tissue of rats with periodontitis. |
1: synthetic cannabinoid methanandamide (Meth-AEA); 2: LPS/(Meth-AEA); 3: LPS | No treatment | 24 specimens | 6 weeks |
| Abidia et al. [106] | Cannabinoid | In vitro study | Human Periodontal fibroblast (HPLF) | cannabinoid compounds (10−4–10−6.5 Min cell culture | The cannabinoids inhibited LPS, TNF-α, IL-1β expression in hPDLFs though CB2R ligands receptors |
cannabinoid (10−4–10−6.5 M) [EC50] | - | 1 h | |
| Lanza Cariccio et al. [108] | Endocannabinoid | In vitro study | Periodontal fibroblasts | Cells culture | Higher survival capacity and neuronal differentiation potential of hPDLSCs treated with Moringin and Cannabidiol |
Moringin (MOR) and Cannabidiol (CBD), |
No treatment | - | 24 h, 48 h and 72 h |
| Nakajima et al. [107] | Endocannabinoid | In vitro study | human gingival fibroblasts (HGFs) | Cells culture | AEA blocked of LPS-triggered NF-jB activation related to hyperinflammatory response in periodontitis. |
Anandamide (AEA)/LPS in different concentrations (0, 1µM, 5µM and 10 µM) | - | - | 48 h |