Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (767 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A type of osteochondritis in which articular cartilage and associated bone becomes partially or totally detached to form joint loose bodies. Affects mainly the knee, ankle, and elbow joints.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Dissecans, Osteochondritis.
Where it fits in the MeSH classification
- Broader topics
- Osteochondritis
Research landscape
PubMed indexes 1,906 records tagged with the MeSH heading “Osteochondritis Dissecans” (counts retrieved 2026-11-04). 299 of them (15.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 590 records.
Reviews account for 314 records (16.5%) and meta-analyses for 7. Randomized controlled trials number 7 (0.4%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 590 |
| 2000-2009 | 455 |
| 2010-2019 | 562 |
| 2020 onward | 299 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 314 | 16.5% |
| Meta-analyses | 7 | 0.4% |
| Randomized controlled trials | 7 | 0.4% |
Method: PubMed query "Osteochondritis Dissecans"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in bones, joints, muscles and skin
Joint, bone, muscle and skin conditions are often judged by pain scores, function questionnaires, imaging or photographs, and symptoms can fluctuate, so placebo response and natural improvement matter. Imaging changes are common in people without symptoms. Nothing on this page is advice about treatment. Check how outcomes were measured, whether the comparison group received a placebo or usual care, and how long the benefit lasted.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Donor-site morbidity after osteochondral autologous transplantation for osteochondritis dissecans of the capitellum: a systematic review and meta-analysis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- PurposeTo determine the rate of donor-site morbidity after osteochondral autologous transplantation (OATS) for capitellar osteochondritis dissecans.
- Closing excerpt
- Level of evidenceLevel IV, systematic review of level IV studies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (236 words)
PurposeTo determine the rate of donor-site morbidity after osteochondral autologous transplantation (OATS) for capitellar osteochondritis dissecans.MethodsA literature search was performed in PubMed/MEDLINE, Embase, and Cochrane Library to identify studies up to November 6, 2016. Criteria for inclusion were OATS for capitellar osteochondritis dissecans, reported outcomes related to donor sites, ≥10 patients, ≥1 year follow-up, and written in English. Donor-site morbidity was defined as persistent symptoms (≥1 year) or cases that required subsequent intervention. Patient and harvest characteristics were described, as well as the rate of donor-site morbidity. A random effects model was used to calculate and compare weighted group proportions.ResultsEleven studies including 190 patients were included. In eight studies, grafts were harvested from the femoral condyle, in three studies, from either the 5th or 6th costal-osteochondral junction. The average number of grafts was 2 (1-5); graft diameter ranged from 2.6 to 11 mm. In the knee-to-elbow group, donor-site morbidity was reported in 10 of 128 patients (7.8%), knee pain during activity (7.0%) and locking sensations (0.8%). In the rib-to-elbow group, one of 62 cases (1.6%) was complicated, a pneumothorax. The proportion in the knee-to-elbow group was 0.04 (95% CI 0.0-0.15), and the proportion in the rib-to-elbow group was 0.01 (95% CI 0.00-0.06). There were no significant differences between both harvest techniques (n.s.).ConclusionsDonor-site morbidity after OATS for capitellar osteochondritis dissecans was reported in a considerable group of patients.Level of evidenceLevel IV, systematic review of level IV studies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28391550 · DOI · PMC5489608
Type IX collagen gene mutations can result in multiple epiphyseal dysplasia that is associated with osteochondritis dissecans and a mild myopathy [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Multiple epiphyseal dysplasia (MED) is a clinically variable and genetically heterogeneous disease that is characterized by mild short stature and early onset osteoarthritis.
- Closing excerpt
- (c) 2010 Wiley-Liss, Inc.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (146 words)
Multiple epiphyseal dysplasia (MED) is a clinically variable and genetically heterogeneous disease that is characterized by mild short stature and early onset osteoarthritis. Autosomal dominant forms are caused by mutations in the genes that encode type IX collagen, cartilage oligomeric matrix protein, and matrilin-3: COL9A1, COL9A2, COL9A3, COMP, and MATN3, respectively. Splicing mutations have been identified in all three genes encoding type IX collagen and are restricted to specific exons encoding an equivalent region of the COL3 domain in all three alpha(IX) chains. MED has been associated with mild myopathy in some families, in particular one family with a COL9A3 mutation and two families with C-terminal COMP mutations. In this study we have identified COL9A2 mutations in two families with MED that also have osteochondritis dissecans and mild myopathy. This study therefore extends the range of gene-mutations that can cause MED-related myopathy. (c) 2010 Wiley-Liss, Inc.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 20358595 · DOI · PMC3557369
Osteochondritis dissecans of the elbow: excellent results in teenage athletes treated by arthroscopic debridement and microfracture [3]
Abstract reading summary — source excerpts
- Opening excerpt
- AimTo evaluate the outcome of patients who underwent microfracture procedure on osteochondritis dissecans (OCD) lesions in the elbow, which had already been proven successful on OCD lesions in the knee and ankle.
- Closing excerpt
- ConclusionsWe advocate arthroscopic microfracturing, followed by a strict rehabilitation regime, as a highly effective treatment for OCD of the humeral capitellum.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (185 words)
AimTo evaluate the outcome of patients who underwent microfracture procedure on osteochondritis dissecans (OCD) lesions in the elbow, which had already been proven successful on OCD lesions in the knee and ankle.MethodsNine young patients who were previously treated by arthroscopic debridement and microfracture by a single surgeon were included in the study. The median age at operation was 15 years (range 12-19). The median time between the procedure and evaluation was 5 years (range 2-9). The evaluation included physical examination and patient interview with elbow function scoring. Success of treatment was determined according evaluation Mayo Elbow Performance Index scores and the patients' return to sports.ResultsEight patients scored excellent results and 1 scored a good result. Four out of 9 patients were able to increase their training intensity, 2 returned to the same level of activity, 2 changed sports (due to reasons unrelated to the health of their elbow), and 1 left professional sports and started training only recreationally. No patients stopped participating in sports altogether.ConclusionsWe advocate arthroscopic microfracturing, followed by a strict rehabilitation regime, as a highly effective treatment for OCD of the humeral capitellum.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 22351577 · DOI · PMC3284183
Research progress of short stature and advanced bone age, early-onset osteoarthritis and osteochondritis dissecans (SSOAOD) caused by acan gene mutation [4]
Abstract reading summary — source excerpts
- Opening excerpt
- IntroductionHeterozygous mutations in the ACAN gene are a key genetic cause of non-syndromic familial short stature.
- Closing excerpt
- Future multicenter, long-term follow-up studies are needed to further clarify the molecular mechanisms of ACAN haploinsufficiency, assess the long-term articular effects of rhGH therapy, and establish early identification criteria, thereby providing a basis for developing targeted therapies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (200 words)
IntroductionHeterozygous mutations in the ACAN gene are a key genetic cause of non-syndromic familial short stature. The associated disease spectrum includes short stature, advanced bone age, early-onset osteoarthritis, and osteochondritis dissecans (SSOAOD). The clinical phenotype is highly heterogeneous, ranging from isolated short stature to severe skeletal developmental abnormalities, reflecting a continuous pathological process from growth plate dysfunction to premature joint degeneration.MethodsThis summary synthesizes current clinical evidence and management approaches for ACAN-related short stature. Recombinant human growth hormone (rhGH) is the primary treatment used to improve height in affected children. Clinical management also integrates growth promotion, joint protection, genetic counseling, and screening of at-risk family members.ResultsrhGH therapy provides moderate improvement in height, but its efficacy decreases with increasing age. Long-term safety of rhGH on joint health remains unclear. The disease spectrum illustrates progressive severity from short stature alone to significant skeletal and joint pathology.DiscussionClinical care should adopt a multidisciplinary approach combining growth promotion, joint protection, and genetic counseling, including screening for at-risk family members. Future multicenter, long-term follow-up studies are needed to further clarify the molecular mechanisms of ACAN haploinsufficiency, assess the long-term articular effects of rhGH therapy, and establish early identification criteria, thereby providing a basis for developing targeted therapies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42255433 · DOI · PMC13233341
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The basic science of the subchondral bone [5]
- Research article Management of osteochondritis dissecans of the knee: current concepts review [6]
- Research article Treatment strategies in osteochondral defects of the talar dome: a systematic review [7]
- Research article Systematic review of treatment strategies for osteochondral defects of the talar dome [8]
- Research article A review of knowledge in osteochondritis dissecans: 123 years of minimal evolution from König to the ROCK study group [9]
- Research article Treatment principles for osteochondral lesions in foot and ankle [10]
References
- Bexkens R, Ogink PT, Doornberg JN, Kerkhoffs GMMJ, Eygendaal D, Oh LS, et al.. Donor-site morbidity after osteochondral autologous transplantation for osteochondritis dissecans of the capitellum: a systematic review and meta-analysis. . 2017. PMID 28391550 · DOI · PMC5489608
- Jackson GC, Marcus-Soekarman D, Stolte-Dijkstra I, Verrips A, Taylor JA, Briggs MD. Type IX collagen gene mutations can result in multiple epiphyseal dysplasia that is associated with osteochondritis dissecans and a mild myopathy. . 2010. PMID 20358595 · DOI · PMC3557369
- Bojanić I, Smoljanović T, Dokuzović S. Osteochondritis dissecans of the elbow: excellent results in teenage athletes treated by arthroscopic debridement and microfracture. . 2012. PMID 22351577 · DOI · PMC3284183
- Chen Y, Wu S, Gu W. Research progress of short stature and advanced bone age, early-onset osteoarthritis and osteochondritis dissecans (SSOAOD) caused by acan gene mutation. . 2026. PMID 42255433 · DOI · PMC13233341
- Madry H, van Dijk CN, Mueller-Gerbl M. The basic science of the subchondral bone. Knee Surg Sports Traumatol Arthrosc. 2010. PMID 20119671 · DOI
- Kocher MS, Tucker R, Ganley TJ, Flynn JM. Management of osteochondritis dissecans of the knee: current concepts review. Am J Sports Med. 2006. PMID 16794036 · DOI
- Tol JL, Struijs PA, Bossuyt PM, Verhagen RA, van Dijk CN. Treatment strategies in osteochondral defects of the talar dome: a systematic review. Foot Ankle Int. 2000. PMID 10694023 · DOI
- Verhagen RA, Struijs PA, Bossuyt PM, van Dijk CN. Systematic review of treatment strategies for osteochondral defects of the talar dome. Foot Ankle Clin. 2003. PMID 12911238 · DOI
- Edmonds EW, Polousky J. A review of knowledge in osteochondritis dissecans: 123 years of minimal evolution from König to the ROCK study group. Clin Orthop Relat Res. 2013. PMID 22362466 · DOI · PMC3586043
- Badekas T, Takvorian M, Souras N. Treatment principles for osteochondral lesions in foot and ankle. Int Orthop. 2013. PMID 23982639 · DOI · PMC3764304
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.