Evidence map›Paper›PMID 34703508›Full record

ReviewThe Japanese dental science review2021

Mechanism of alveolar bone destruction in periodontitis - Periodontal bacteria and inflammation.

Michihiko Usui, Satoru Onizuka, Tsuyoshi Sato, Shoichiro Kokabu, Wataru Ariyoshi, Keisuke Nakashima

Open access · goldAbstract readReview
In one paragraph

Review in The Japanese dental science review, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 3 pooled it
17.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

128 citing papers in PubMed, 3 syntheses or guidelines pooled it, 196 citations in OpenAlex.

  1. Pooled it
  2. Is Obesity a Risk Factor for Periodontal Disease in Adults? A Systematic Review.International journal of environmental research and public health · 2022
    Pooled it
  3. Pooled it
  4. Trial
  5. Characterizing the supragingival microbiome of healthy pregnant women.Frontiers in cellular and infection microbiology · 2022
    Trial
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

68 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Michihiko UsuiDivision of Periodontology, Department of Oral Function, Kyushu Dental University, 2-6-1 Manazuru, Kokurakita-ku, Kitakyushu, Fukuoka 803-8580, Japan.
Satoru OnizukaDivision of Periodontology, Department of Oral Function, Kyushu Dental University, 2-6-1 Manazuru, Kokurakita-ku, Kitakyushu, Fukuoka 803-8580, Japan.
Tsuyoshi SatoDepartment of Oral and Maxillofacial Surgery, Saitama Medical University, 38 Moro-hongou, Moroyama-machi, Iruma-gun, Saitama 350-0495, Japan.
Shoichiro KokabuDivision of Molecular Signaling and Biochemistry, Department of Health Promotion, Kyushu Dental University, Kokurakita-ku, Kitakyushu, Fukuoka 803-8580, Japan.
Wataru AriyoshiDivision of Infection and Molecular Biology, Department of Health Improvement, Kyushu Dental University, 2-6-1 Manazuru, Kokurakita-ku, Kitakyushu, Fukuoka 803-8580, Japan.
Keisuke NakashimaDivision of Periodontology, Department of Oral Function, Kyushu Dental University, 2-6-1 Manazuru, Kokurakita-ku, Kitakyushu, Fukuoka 803-8580, Japan.
Kyushu Dental University · JPSaitama Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Periodontal disease is an inflammatory disease caused by periodontopathogenic bacteria, which eventually leads to bone tissue (alveolar bone) destruction as inflammation persists. Periodontal tissues have an immune system against the invasion of these bacteria, however, due to the persistent infection by periodontopathogenic bacteria, the host innate and acquired immunity is impaired, and tissue destruction, including bone tissue destruction, occurs. Osteoclasts are essential for bone destruction. Osteoclast progenitor cells derived from hematopoietic stem cells differentiate into osteoclasts. In addition, bone loss occurs when bone resorption by osteoclasts exceeds bone formation by osteoblasts. In inflammatory bone disease, inflammatory cytokines act on osteoblasts and receptor activator of nuclear factor-κB ligand (RANKL)-producing cells, resulting in osteoclast differentiation and activation. In addition to this mechanism, pathogenic factors of periodontal bacteria and mechanical stress activate osteoclasts and destruct alveolar bone in periodontitis. In this review, we focused on the mechanism of osteoclast activation in periodontitis and provide an overview based on the latest findings.

Indexed as

InflammationKeystone pathogen hypothesisOsteoclastPeriodontal bacteriaPeriodontitisRANKL

Identifiers

PMID34703508
PMCPMC8524191
OpenAlexW3207493014

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.