Are inflammatory cells increased in painful human tendinopathy? A systematic review.
Br J Sports Med
; 50(4): 216-20, 2016 Feb.
Article
en En
| MEDLINE
| ID: mdl-26246419
ABSTRACT
BACKGROUND:
The role of inflammation in tendinopathy has historically been a subject of significant controversy. Our primary aim was to determine whether inflammatory cell numbers were increased in painful human tendinopathy versus healthy control tendons. Our secondary aim was to assess whether the inflammatory cells had been linked with symptoms or disease stage.METHODS:
We conducted a systematic review of the scientific literature using the PRISMA and Cochrane guidelines of the Medline database using specific search criteria. Only studies measuring inflammatory cells using specific markers in tissue from human patients with the clinical diagnosis of tendinopathy were included. Inclusion was agreed on by 2 independent researchers on review of abstracts or full-text using specific predetermined criteria. The search yielded 5 articles in total.RESULTS:
There were increased numbers of macrophages (4 studies) and mast cells (3 studies) in tendinopathic versus healthy control tissues. One study demonstrated increased numbers of T cells in tendinopathic tissue versus healthy control tendons. There were reduced numbers of T cells (1 study), macrophages (2 studies) and mast cells (2 studies) in torn tendon versus intact tendinopathic tissue.CONCLUSIONS:
The existing evidence supports the hypothesis that increased numbers of inflammatory cells are present in pathological tendons. The lack of high-quality quantitative studies in this area demonstrates a clear need for future research to better understand the role of inflammation in tendinopathy.Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Mastocitosis Sistémica
/
Tendinopatía
/
Dolor Musculoesquelético
/
Macrófagos
Tipo de estudio:
Guideline
/
Systematic_reviews
Límite:
Humans
Idioma:
En
Revista:
Br J Sports Med
Año:
2016
Tipo del documento:
Article
País de afiliación:
Reino Unido