Evidence map›Paper›PMID 40251915›Full record

ReviewOrthodontics & craniofacial research2025

Mandibular Condylar Cartilage in Development and Diseases: A PTHrP-Centric View.

Chiaki Tsutsumi-Arai, Amy Tran, Yuki Arai, Wanida Ono, Noriaki Ono

Abstract readReview
In one paragraph

Review in Orthodontics & craniofacial research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Association ofInternational journal of molecular sciences · 2026
    Article
  2. Article
  3. Neural Orchestration of Mandibular Development.International dental journal · 2026
    Review
  4. Review
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

5 authors.

Chiaki Tsutsumi-AraiUniversity of Texas Health Science Center at Houston School of Dentistry, Houston, Texas, USA.
Amy TranUniversity of Texas Health Science Center at Houston School of Dentistry, Houston, Texas, USA.
Yuki AraiUniversity of Texas Health Science Center at Houston School of Dentistry, Houston, Texas, USA.
Wanida OnoUniversity of Texas Health Science Center at Houston School of Dentistry, Houston, Texas, USA.
Noriaki OnoUniversity of Texas Health Science Center at Houston School of Dentistry, Houston, Texas, USA.ORCID https://orcid.org/0000-0002-3771-8230

Funding

Skeletal stem cell plasticity in craniofacial bone diseases.R35DE034348 · NIDCR · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI Noriaki Ono · 2024 to 2026
$3.1M
Craniofacial skeletal cell lineage plasticity for reconstituting stem cells and their nichesR01DE030630 · NIDCR · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ONO, NORIAKI, ONO, WANIDA · 2021 to 2025
$2.2M
Pharmacological rescue of tooth eruption disordersR01DE030416 · NIDCR · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI Wanida Ono · 2023 to 2026
$1.9M
NIDCR NIH HHS R01 DE030416NIDCR NIH HHS R01DE030416NIDCR NIH HHS R01 DE030630NIDCR NIH HHS R01DE030630NIDCR NIH HHS R35 DE034348NIDCR NIH HHS R35DE034348
6 · The paper itself

Abstract

The mandibular condylar cartilage (MCC) is a dual-function component of the temporomandibular joint (TMJ), acting as both articular cartilage for jaw movement and growth cartilage for vertical growth of the mandibular condyle. Parathyroid hormone-related protein (PTHrP) plays a critical role in orchestrating chondrogenesis in the long bone, and its importance is also highlighted in both MCC development and TMJ function. Here, we discuss the role of PTHrP in the development, growth and diseases of the MCC. PTHrP is a key morphogen in the MCC that regulates chondrogenesis by promoting chondrocyte proliferation and preventing premature hypertrophic differentiation. Exclusively expressed in the superficial layer, PTHrP diffuses across the MCC and targets chondrocytes in deeper layers, regulating transcription factors such as RUNX2 and SOX9. PTHrP regulates chondrocyte differentiation through two main pathways: the PTHrP-PTH1R signalling pathway, which suppresses hypertrophy and the PTHrP-Ihh negative feedback loop, which balances proliferation and hypertrophy. In the postnatal murine MCC, PTHrP levels are high early on and decrease after the onset of mastication around P21. Altered mechanical environments, such as those therapeutically induced as mandibular advancement, increase PTHrP expression, promoting chondrocyte proliferation and delaying hypertrophy. PTHrP also plays a dual role in adult TMJ diseases, particularly in osteoarthritis (OA); PTHrP expression transiently increases during the early stages of TMJ-OA to promote cell proliferation, but its eventual decrease contributes to the progression of the disease. This highlights the complex role of PTHrP in maintaining MCC homeostasis and its potential involvement in TMJ-OA pathology. The MCC combines the characteristics of growth and articular cartilage and functions distinctively in three phases: development before occlusion, growth after the occlusion is established, and maintenance after the growth is complete. While PTHrP plays a multifaceted role in all phases, further research is needed to fully understand how it regulates MCC development, growth and diseases.

Indexed as

Cartilage, ArticularMandibular CondyleParathyroid Hormone-Related ProteinTemporomandibular Joint DisordersAnimalsCell DifferentiationCell ProliferationChondrocytesChondrogenesisHumansOsteoarthritisSignal TransductionTemporomandibular JointParathyroid Hormone-Related Proteinmandibular condylar cartilageparathyroid hormone‐related proteintemporomandibular jointtemporomandibular joint osteoarthritis

Identifiers

PMID40251915
PMCPMC12755033

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.