Effects of aloe-emodin on alveolar bone in <i>Porphyromonas gingivalis</i>-induced periodontitis rat model: a pilot study

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Abstract

Purpose

Aloe-emodin (AE), a natural anthraquinone abundant in aloe plants and rhubarb ( Rheum rhabarbarum), has long been used to treat chronic inflammatory diseases. However, AE’s underlying mechanisms in periodontal inflammation have not been fully elucidated. Acidic mammalian chitinase (AMCase) is a potential biomarker involved in bone remodeling. This study aimed to evaluate AE’s effect on periodontitis in rats and investigate AMCase expression.

Methods

Eighteen Sprague-Dawley rats were separated into the following groups: healthy (group 1), disease (group 2), vehicle (group 3), AE high-dose (group 4), and AE low-dose (group 5). Porphyromonas gingivalis ligatures were placed in rats (groups 2–5) for 7 days. Groups 4 and 5 were then treated with AE for an additional 14 days. Saliva was collected from all groups, and probing pocket depth was measured in succession. Periodontal pocket tissues were subjected to histomorphometric analysis after the rats were sacrificed. Bone marrow-derived macrophages and murine macrophages were stimulated with receptor activator of nuclear factor-κB ligand (RANKL) and treated with different concentrations of AE. AMCase expression was detected from the analysis of saliva, periodontal pocket tissues, and differentiated osteoclasts.

Results

Among rats with P. gingivalis-induced periodontitis, the alveolar bone resorption levels and periodontal pocket depth were significantly reduced after treatment with AE. AMCase protein expression was significantly higher in the disease group than in the healthy control ( P<0.05). However, AE inhibited periodontal inflammation by downregulating AMCase expression in saliva and periodontal pocket tissue. AE significantly reduced RANKL-stimulated osteoclastogenesis by modulating AMCase ( P<0.05).

Conclusions

AE decreases alveolar bone loss and periodontal inflammation, suggesting that this natural anthraquinone has potential value as a novel therapeutic agent against periodontal disease.

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Most cited references 36

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Bone resorption by osteoclasts.

S Teitelbaum (2000)

Osteoporosis, a disease endemic in Western society, typically reflects an imbalance in skeletal turnover so that bone resorption exceeds bone formation. Bone resorption is the unique function of the osteoclast, and anti-osteoporosis therapy to date has targeted this cell. The osteoclast is a specialized macrophage polykaryon whose differentiation is principally regulated by macrophage colony-stimulating factor, RANK ligand, and osteoprotegerin. Reflecting integrin-mediated signals, the osteoclast develops a specialized cytoskeleton that permits it to establish an isolated microenvironment between itself and bone, wherein matrix degradation occurs by a process involving proton transport. Osteopetrotic mutants have provided a wealth of information about the genes that regulate the differentiation of osteoclasts and their capacity to resorb bone.

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Staging and grading of periodontitis: Framework and proposal of a new classification and case definition.

Maurizio Tonetti, Henry Greenwell, Kenneth S Kornman (2018)

Authors were assigned the task to develop case definitions for periodontitis in the context of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. The aim of this manuscript is to review evidence and rationale for a revision of the current classification, to provide a framework for case definition that fully implicates state-of-the-art knowledge and can be adapted as new evidence emerges, and to suggest a case definition system that can be implemented in clinical practice, research and epidemiologic surveillance.

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The molecular understanding of osteoclast differentiation.

Masataka Asagiri, Hiroshi Takayanagi (2007)

Osteoclasts are multinucleated cells of monocyte/macrophage origin that degrade bone matrix. The differentiation of osteoclasts is dependent on a tumor necrosis factor (TNF) family cytokine, receptor activator of nuclear factor (NF)-kappaB ligand (RANKL), as well as macrophage colony-stimulating factor (M-CSF). Congenital lack of osteoclasts causes osteopetrosis, investigation of which has provided insights into the essential molecules for osteoclastogenesis, including TNF receptor-associated factor (TRAF) 6, NF-kappaB and c-Fos. In addition, genome-wide screening techniques have shed light on an additional set of gene products such as nuclear factor of activated T cells (NFAT) c1. Here we summarize the efforts to understand the sequential molecular events induced by RANKL during osteoclast differentiation. RANKL binds to its receptor RANK, which recruits adaptor molecules such as TRAF6. TRAF6 activates NF-kappaB, which is important for the initial induction of NFATc1. NFATc1 is activated by calcium signaling and binds to its own promoter, thus switching on an autoregulatory loop. An activator protein (AP)-1 complex containing c-Fos is required for the autoamplification of NFATc1, enabling the robust induction of NFATc1. Finally, NFATc1 cooperates with other transcriptional partners to activate osteoclast-specific genes. NFATc1 autoregulation is controlled by an epigenetic mechanism, which has profound implications for an understanding of the general mechanism of irreversible cell fate determination. From the clinical point of view, RANKL signaling pathway has promise as a strategy for suppressing the excessive osteoclast formation characteristic of a variety of bone diseases.

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Author and article information

Journal

Journal ID (nlm-ta): J Periodontal Implant Sci

Journal ID (iso-abbrev): J Periodontal Implant Sci

Journal ID (publisher-id): JPIS

Title: Journal of Periodontal & Implant Science

Publisher: Korean Academy of Periodontology

ISSN (Print): 2093-2278

ISSN (Electronic): 2093-2286

Publication date Collection: October 2022

Publication date (Electronic): 09 May 2022

Volume: 52

Issue: 5

Pages: 383-393

Affiliations

[1 ]Department of Periodontology, School of Dentistry, Jeonbuk National University, Jeonju, Korea.

[2 ]Department of Periodontology, School of Dentistry, Beihua University, Jilin, China.

[3 ]Department of Dental Pharmacology, School of Dentistry, Jeonbuk National University, Jeonju, Korea.

[4 ]Laboratory of Pharmacology, School of Pharmacy and Institute of New Drug Development, Jeonbuk National University, Jeonju, Korea.

[5 ]Research Institute of Clinical Medicine of Jeonbuk National University, Jeonju, Korea.

Author notes

Correspondence: Seok-Mo Heo. Department of Periodontology, School of Dentistry, Jeonbuk National University, 567 Baekje-daero, Deokjin-gu, Jeonju 54896, Korea. neoheo@ 123456jbnu.ac.kr , Tel: +82-63-250-2018, Fax: +82-63-250-2259

Correspondence: Yunjo Soh. Laboratory of Pharmacology, School of Pharmacy and Institute of New Drug Development, Jeonbuk National University, 567 Baekje-daero, Deokjin-gu, Jeonju 54896, Korea. ysoh@ 123456jbnu.ac.kr , Tel: +82-63-270-4037, Fax: +82-63-270-4038

Key finding: Aloe-emodin can decrease alveolar bone resorption and periodontal inflammation.

Author information

Ming Yang https://orcid.org/0000-0002-1794-5401

Saroj K Shrestha https://orcid.org/0000-0002-8932-3468

Yunjo Soh https://orcid.org/0000-0001-9543-225X

Seok-Mo Heo https://orcid.org/0000-0002-2511-8123

Article

DOI: 10.5051/jpis.2104060203

PMC ID: 9614176

PubMed ID: 36302645

SO-VID: 60c95c7c-19f9-4a0d-8acf-b14df03812b7

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( https://creativecommons.org/licenses/by-nc/4.0/).

History

Date received : 26 July 2021

Date revision received : 27 March 2022

Date accepted : 04 April 2022

Funding

Funded by: Biomedical Research Institute, Jeonbuk National University Hospital, CrossRef https://doi.org/10.13039/100016988;

Funded by: Ministry of Trade, Industry and Energy, CrossRef https://doi.org/10.13039/501100003052;

Award ID: 20012892

Funded by: National Research Foundation of Korea, CrossRef https://doi.org/10.13039/501100003725;

Award ID: NRF-2021R1I1A3055927

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Effects of aloe-emodin on alveolar bone in Porphyromonas gingivalis-induced periodontitis rat model: a pilot study

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Arab Journal of Forensic Sciences & Forensic Medicine (AJFSFM)

Most cited references 36

Bone resorption by osteoclasts.

Staging and grading of periodontitis: Framework and proposal of a new classification and case definition.

The molecular understanding of osteoclast differentiation.

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