Patellar tendon morphology in volleyball
athletes with and without patellar tendinopathy.
athletes with and without patellar tendinopathy.
Kulig K, Chang TJ, Hannanvash
N, Reischl SF, Song P, and Bashord GR. Scand J Med Sci Sports. 2012: 1-8.
N, Reischl SF, Song P, and Bashord GR. Scand J Med Sci Sports. 2012: 1-8.
Patellar tendinopathy is common in athletics, especially among
volleyball players. The condition occurs due to degeneration and/or
inflammation secondary to physical activity. Additionally, clinical imaging
struggles to distinguish between inflammatory and degenerative conditions
further complicating diagnosis and thus, management. Therefore, Kulig and
colleagues sought to perform a detailed analysis of patellar tendon collagen
bundle organization in elite male volleyball athletes. The authors recruited 94
male participants (10 controls and 84 NCAA Division I or Olympic volleyball
players) over 6 feet tall. The 84 volleyball players were divided into those
with anterior knee pain near the patellar tendon (symptomatic, 44 players) and
those without (asymptomatic, 40 players). All participants completed a VISA-P
questionnaire (lower VISA-P score indicated more pain and restrictions).
Furthermore, the researchers collected anthropometric data (body mass, height,
etc.) and conducted personal interviews. Lastly, the researchers performed B-mode ultrasound imaging to assess the collagen organization
and thickness of the patellar tendons. While B-mode ultrasound cannot
specifically identify inflammation, the researchers considered inflammation to
be the cause of the tendinopathy if the athlete was symptomatic, yet did not demonstrate
collagen disorganization, thus ruling out degenerative changes to the tendon.
Overall, patellar tendons of asymptomatic athletes, and athletes with
tendinopathy, demonstrated greater proximal tendon thicknesses compared to
control participants; however VISA-P scores were significantly lower in
symptomatic athletes than asymptomatic athletes. Symptomatic athletes also had
greater collagen bundle disorganization (degeneration) compared to both control
participants and asymptomatic volleyball players.
volleyball players. The condition occurs due to degeneration and/or
inflammation secondary to physical activity. Additionally, clinical imaging
struggles to distinguish between inflammatory and degenerative conditions
further complicating diagnosis and thus, management. Therefore, Kulig and
colleagues sought to perform a detailed analysis of patellar tendon collagen
bundle organization in elite male volleyball athletes. The authors recruited 94
male participants (10 controls and 84 NCAA Division I or Olympic volleyball
players) over 6 feet tall. The 84 volleyball players were divided into those
with anterior knee pain near the patellar tendon (symptomatic, 44 players) and
those without (asymptomatic, 40 players). All participants completed a VISA-P
questionnaire (lower VISA-P score indicated more pain and restrictions).
Furthermore, the researchers collected anthropometric data (body mass, height,
etc.) and conducted personal interviews. Lastly, the researchers performed B-mode ultrasound imaging to assess the collagen organization
and thickness of the patellar tendons. While B-mode ultrasound cannot
specifically identify inflammation, the researchers considered inflammation to
be the cause of the tendinopathy if the athlete was symptomatic, yet did not demonstrate
collagen disorganization, thus ruling out degenerative changes to the tendon.
Overall, patellar tendons of asymptomatic athletes, and athletes with
tendinopathy, demonstrated greater proximal tendon thicknesses compared to
control participants; however VISA-P scores were significantly lower in
symptomatic athletes than asymptomatic athletes. Symptomatic athletes also had
greater collagen bundle disorganization (degeneration) compared to both control
participants and asymptomatic volleyball players.
The presence of collagen
bundle disorganization and lower VISA-P scores suggests that symptoms of
tendinopathy are associated with tendon degeneration rather than inflammatory
responses, although all athletes displayed morphological changes to the tendon
compared to control participants. While interesting one should be cautious not
to generalize these findings to the general population. The current study
observed only elite male volleyball players. These athletes may be unique
because of their high volume of training, which may explain why athletes had
thicker tendons than control participants. In order to increase
generalizability, future research should compare various levels of competition
(recreational, high school) and sports to healthy controls. Further, it would
be interesting to follow athletes over time to determine when and how certain
aspects of training begin to induce healthy adaptation (thickness) and
degenerative changes. Eventually, this data conceivably could optimize training
regiments for volleyball athletes so as to prevent tendinopathy from occurring.
In the meantime, given this information, clinicians should be aware that
volleyball athletes (as well as possibly other athletes) who present with recurrent
patellar tendon pain may be experiencing tendonosis rather than tendonitis and
could respond to a change in treatment approach. Tell us what you think. Have
you seen athletes which, given this information may be experiencing patellar
tendonosis rather than tendonitis? Further, do you see this evidence changing
how you treat tendinopathies which may be degenerative changes more so than
inflammatory change?
bundle disorganization and lower VISA-P scores suggests that symptoms of
tendinopathy are associated with tendon degeneration rather than inflammatory
responses, although all athletes displayed morphological changes to the tendon
compared to control participants. While interesting one should be cautious not
to generalize these findings to the general population. The current study
observed only elite male volleyball players. These athletes may be unique
because of their high volume of training, which may explain why athletes had
thicker tendons than control participants. In order to increase
generalizability, future research should compare various levels of competition
(recreational, high school) and sports to healthy controls. Further, it would
be interesting to follow athletes over time to determine when and how certain
aspects of training begin to induce healthy adaptation (thickness) and
degenerative changes. Eventually, this data conceivably could optimize training
regiments for volleyball athletes so as to prevent tendinopathy from occurring.
In the meantime, given this information, clinicians should be aware that
volleyball athletes (as well as possibly other athletes) who present with recurrent
patellar tendon pain may be experiencing tendonosis rather than tendonitis and
could respond to a change in treatment approach. Tell us what you think. Have
you seen athletes which, given this information may be experiencing patellar
tendonosis rather than tendonitis? Further, do you see this evidence changing
how you treat tendinopathies which may be degenerative changes more so than
inflammatory change?
Written by: Kyle Harris
Reviewed by: Laura McDonald
Related Posts:
Kulig K, Landel R, Chang YJ, Hannanvash N, Reischl SF, Song P, & Bashford GR (2012). Patellar tendon morphology in volleyball athletes with and without patellar tendinopathy. Scandinavian Journal of Medicine & Science in Sports PMID: 23253169
it is widely accepted that tendinopathy is always degenerative. a short lived inflammatory event may precede the degenarative tendon change according to some (fredberg) but there is little evidence of this in the literature, by way of the absence of inflammatory cells.
a conventional inflammatory event characterised by prostaglandins etc will occur during partial or complete rupture.
the debate continues when we consider that neurogenic chemicals are released by tenocytes in tendinopathic states, such as glutamate, substance P etc (read danielson, andersson, alfredson).
these are also present in inflammatory events, but they also upregulate after activity!! and there are cytokines which will also act in an autocrine and paracrine mode on tenocytes. so do we have neurogenic inflammation? can we call it inflammation in the absence of inflammatory cells? is it pathological given that it occurs following activity? many questions still to be answered.
cook and purdam in bjsm proposed a model for continuum of pathogenesis, from the early reactive tendon where proteoglycan expression changes leading to matrix disruption(supported by corps et al and samiric et al)to the fully blown tendinosis stage, which can be irreversible.
adaptive preconditioning for the tendon is an attractive idea, but there are many factors including genetics (collins, september), affecting tendinopathy…so the search continues…as it would be naive to think that this alone could prevent the development of pathology. having said that, any event that can reduce the potentially damaging forces going though the tendon could be helpful, at least intuitively.
feel free to contact me for further information.
best wishes to all
Arturo thanks for the comment! You are right that tendinopathy is commonly thought to be degenerative in nature but previous work from Perry et al.(https://www.ncbi.nlm.nih.gov/pubmed/15726091) has found an increased gene expression of inflammatory markers (COX-2 & FLAP) following overuse training of the rotator cuff in a rat model.
I agree that the presence of neurogenic factors are commonly found in tendinopathic tendons and can be related to the increase in pain levels.
You bring up a great point when talking about proteoglycans and tendinopathy. This is an area that is often overlooked but very important for the pathogenesis of tendinopathy. Previous studies have found an increased expression (https://www.ncbi.nlm.nih.gov/pubmed/17318892) and deposition (https://www.ncbi.nlm.nih.gov/pubmed/21688311) of large proteoglycans that are commonly found in cartilage and not tendon following overuse. This suggests that overuse is causes a switch from a tenocyte to a chondrocyte phenotype. This is very problematic since tendons need to resist tensile loads and will not be able to function optimally thereby being at risk for partial or complete tears.
Clinically there are several things that may help reverse this degenerative state (tenocyte to chondrocyte). First it has been shown in a rat model that rest (https://www.ncbi.nlm.nih.gov/pubmed/18459028) will reverse this process. Also in a recent study presented at the ORS (https://www.ors.org/Transactions/59/PS2–071/1360.html) this year that low level exercise following overuse can improve tendon protein expression. There is clearly much more research required however these are two options to currently help our athletes.
This new review article is particularly relevant to this discussion https://bjsm.bmj.com/content/early/2013/03/08/bjsports-2012-091957.full