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hmm.. depends. Are you exclusively infiltrating CS or are you injecting a cocktail?

Assuming that you are thinking of local anesthetic as the other component; just wondering why would that make any difference to CS effect on "inflammation" other than if using same dose increasing volume and diluting concentration of CS?

Cheers

Martin

Foot and Ankle Clinic
1365 Grant Ave.
Winnipeg Manitoba R3M 1Z8
phone [204] 837 FOOT (3668)
fax [204] 774 9918
www.winnipegfootclinic.com

[quote=Mart;265938]Assuming that you are thinking of local anesthetic as the other component; just wondering why would that make any difference to CS effect on "inflammation" other than if using same dose increasing volume and diluting concentration of CS?

Hi Martin..in situations like this I ALWAYS play it safe and say 'I don't know". Got me out of a lot of trouble in the past..

however.. diluting Dexamethasone with LA, which here at least is routine practice, may well be giving us a false impression that it is the CS that is doing the job in terms of pain relief, rather than the LA, or indeed the medium for the CS which has also been shown to reduce pain.
Also, pain.. or for that matter inflammation, may not necessarily be inflammation cell driven, and so the mechanism of action, and its apparent role in pain relief may infact be mediated by other pathways..

call me crazy!

[quote=toomoon;265948] "Don't know" . . . I must say half a dozen times daily to my patients . . this is good by me too :) . . . just wanted to check I wasn't missing something though.

The evidence from McMillan et al suggests some effect from the CS given its duration of pain reduction and this is consistent with other studies using insoluble CS with longer pain relief.

I think your concern regarding cause of pain is important and have long suspected that may have more than one root in those with chronic plantar fasciosis.

What I find perplexing is that the few with US confirmed chronic plantar fasciosis who I have been able to re-examine and are pain free after one year when re-examined showed no significant change in sonographic appearance. In other words from an ultrasound perspective they appear unchanged. When I started using US I would re-examine patients on 4 and 8 week reviews with US to look for evidence of reduction in degenerative change. I stopped doing this after awhile because in the majority there was no change despite resolution in symptoms. My assumption was simply that there was insufficient time to see any remodelling, however after one year that seems unlikely. What I also find odd is this runs contrary to anything I have seen published; I don't think this is explained by sonographic error on my part.

There is some evidence which suggests that plantar fibromatosis is invoked by cell messaging from adjacent fat. Plantar fibromatosis appears sonographically identical to distal plantar fasciosis unless it is invasive (which is rare)

I have seen rapidly occurring distal plantar fasciosis develop with high suspicion for cause being irritation from rigid foot orthoses

I increasingly wonder if the initiating cause of plantar fasciosis may be irritation to plantar fibro-fatty pad, subsequent signalling which up regulates fibroblast activity in the fascia with increase in ECM and so on. It seems likely that the medial process of calcaneal tuberosity, because of its shape and the nature of foot alignment would be a site of maximal compression stress to the plantar fibro-fatty pad. It is more often than not that the plantar fibro-fatty pad at the medial process of calcaneal tuberosity appears excessively hypoechoic on US when plantar fasciosis is present. This is explained in most texts as being the result of lymphedema ie increased load on normally flattened lymphatics from drainage to adjacent inflamed fascia. This doesn't make sense if there is no neovascularisation; ie no vessels to leak fluid.

This begs the question as to whether the fascia is the pain generator (or perhaps the plantar fibro-fatty pad is) especially since the pain seems to resolve without any change to the sonographic appearance of the fascia.

and you are concerned that people may call you crazy :) ???

Cheers

Martin


Foot and Ankle Clinic
1365 Grant Ave.
Winnipeg Manitoba R3M 1Z8
phone [204] 837 FOOT (3668)
fax [204] 774 9918
www.winnipegfootclinic.com

Mart:

Good posting.

My belief that is we are just don't sufficient knowledge yet to know, for sure, how much of "plantar fasciitis" is inflammatory and how much of "plantar fasciitis" is "fasciosus"to some extent and that not all cases of "plantar fasciitis" should be called "plantar fasciosus". I'm not for making wholesale changes in diagnostic names unless there is concrete evidence that the name change needs to occur. Short acting cortisone's main effect on the human body is a reduction in inflammation. Patient after patient after patient get good temporary relief of less chronic cases of plantar fasciitis with cortisone injections...most likely by reducing inflammation, whether it is within the actual substance of the plantar aponeurosis or within the tissue that surrounds the plantar aponeurosis. Until someone can conclusively prove to me that all cases of what we currently call plantar fasciitis are non-inflammatory in nature, then I will not start making a wholesale change in calling all conditions of this nature "plantar fasciosus".

Maybe the term plantar fascial dysfunction would be a better.

__________________
Sincerely,

Kevin

**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College

e-mail: kevinakirby@comcast.net

Private Practice:
107 Scripps Drive, Suite 200
Sacramento, CA 95825 USA
My location

Voice: (916) 925-8111 Fax: (916) 925-8136
**************************************************

Thanks for the posting Martin.. this is such an interesting topic.

I do not think there is any great surprise that once there has been change to the fascia, it will not revert even in the absence of pain. This is exactly what we see with tendinopathy, and the plantar fascia behaves in a similar manner. I suspect that more than anything this has to do with the relatively greater concentration of Type 3 collagen vs the normal Type 1, with Type 3 collagen being very unlikely to remodel after it is established since it is not designed as much as stress or load accepting material. By far the most abundant collagen in human tissue is type I which accounts for between 65 – 95% of the total collagens. Type I collagen is the major protein of tenon, ligament, bone, skin and intramuscular connective tissue, with small amounts of other types of collagen (types V, III, VII and XIV). Type I collagen is found predominantly in these tissues because it tends to form into parallel fibres which produce high tensile strength and limited elasticity. In tendons and the plantar fascia the fibres are also arranged horizontally and transversely to form spirals and plaits along their course. This type of tissue therefore is eminently suited for force transmission.

In terms of quantity, type III collagen ( or more properly labelled Collagen alpha-1(III) is the second most prevalent. In adult tissue its proportion ranges from 5 – 30% but high proportions exist in foetal and granulation tissue. So, when the ratio of Type III to Type I collagen is abnormally high, the normal parallel bundled fibre structure is disturbed; the continuity of the collagen is lost with disorganized fiber structure and evidence of both collagen repair and collagen degeneration.
Microtears and collagen fibre separations are seen. Many of the collagen fibres are thin, fragile, and separated from each other.
The number of fibroblast cells is increased; the tenocytes look different, with a more blast-like morphology (the cells look thicker, less linear). These differences show that the cells are actively trying to repair the tissue.
Perhaps the major reason for the phenomenon you observe is that when tenocytes are cultured from tendinosis they continue to produce abnormal collagen outside of the body; the tenocytes produced collagen with abnormally high Type III to Type I ratios (as compared to collagen produced by tenocytes cultured from normal tendon). This observation is significant because it shows that the tenocytes have been altered and continue to produce abnormal collagen even when the repetitive or injurious motion is no longer present.
Check out: Maffulli N, Ewen SWB, Waterston SW, et al. Tenocytes from ruptured and tendinopathic Achilles tendons produce greater quantities of Type III collagen than tenocytes from normal Achilles tendons. Am J Sports Med 28(4):499-505, 2000.

Interesting discussion..
best
Simon

Well Dr. Kirby, it does not happen often, but I am afraid I must put forth an opposite view (as distinct from a disagreement). I put forth the following with input from my friend Scott Wearing

I have not looked specifically at corticosteroids for a long time and am probably not the best person to comment.. but I will anyway (;.
Having said that, I seem to recall that generally, they show a positive effect but one that is short lived (~1month) and is often confounded by a powerful response to placebo. For instance, it seems that "needling" without injection may be as effective as injection with corticosteroids in tendinopathies.

In the absence to evidence to the contrary, I assume the pathological pathway to PFitis is probably similar to that of tendinopathy.

So, if I assume that steroids work in some people at least some of the time; then it is possible that PFitis may have a local inflammatory component (at least in some phase(s) of the disease).

Certainly, corticoid steroids are potent anti-inflamm agents that act directly on nuclear steroid receptors to control rate of synthesis of mRNA and proteins. This has a number of consequences, including changes in T and B cell functions, changes in white cell traffic, alterations in levels of cytokines and enzymes, and inhibition of phospholipase A2 resulting in a reduction in proinflammatory derivatives of arachidonic acid (everyone seems to be pinning their hopes on PGE2). Some of these derivatives, such as bradykinin or histamine, can stimulate nociceptive fibres directly while others (prostaglandins, leukotrienes, and interleukins 1 and 6 may sensitise nociceptives to mechanical or other stimuli.

However, based on findings in tendinopathy, it is possible that pain may not be mediated via prostaglandins (ie chemical inflammation). I think it was Alfredson that first demonstrated PGE2 levels were not elevated in tendinopathy but rather neurotransmitters (that were previously thought to be found only in the CNS), such as Glutimate were elevated. Interestingly, glucocorticoids have also recently been shown to suppress synaptic glutamate release (albeit in other tissues), so it is possible that corticosteroid injections may act via this pathway instead via their perceived anti-inflammatory role.

As for the changes in plantar fascial dimensions that have been observed with steroid injection over the short term, these are generally modest (witihin measurement error) and, if I was a betting man, probably related to tissue fluid levels rather than alterations in collagen1.

I tihnk I should probably stop my tirade now - sorry!

Good posting, Simon.

How about "plantar fascial dysfunction" since we really don't know how much of what we currently call "plantar fasciitis" and/or "plantar fasciosus" is inflammatory in nature and how much of it is degenerative in nature?

About time you started contributing more here on something other than barefoot running.....

__________________
Sincerely,

Kevin

**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College

e-mail: kevinakirby@comcast.net

Private Practice:
107 Scripps Drive, Suite 200
Sacramento, CA 95825 USA
My location

Voice: (916) 925-8111 Fax: (916) 925-8136
**************************************************

Haha.. yeah.. I am preparing myself for the day ASICS sacks me and I have nothing to do. I used to be a podiatrist once you know, and plantar heel pain was always my... "Achilles Heel".. boom boom.. because in so many ways what was being taught and the treatment methods never made sense to me.

I still am not sure about the term plantar fascial dysfunction because it really IS the plantar aponeurosis. Seems nitpicking I know, but how come we have to accept this misnomer? If it makes sense to everyone else, then I am ok with it, and it seems that we just cannot shake the global acceptance of the involvement of the "plantar fascia"... maybe I should just conform! I have always just been happy with chronic plantar heel pain. Accurate and descriptive in the absence of an absolute diagnosis.
Guitar tuned, packed and ready to accompany your dulcet tones next week my friend!

s

Simon and Colleagues:

Even though when I do my lecture on the "Ten Functions of the Plantar Fascia" I go into great detail that what we commonly clinically call the "plantar fascia" is actually the "central component of the plantar aponeurosis", I have decided that sometimes I should call this structure the plantar fascia since most clinicians use this term "plantar fascia" to describe the central component of the plantar aponeurosis (CCPA).

However, now having slept on my suggestion of "plantar fascial dysfunction" for one night, I think I will change my mind and suggest that the term "plantar fascial stress syndrome" may, perhaps, be a better name for the myriad of tension stress-related and compression stress-related conditions of the CCPA.

Plantar fascia stress syndrome would include the conditions of:

1. Proximal plantar fasciitis (i.e. plantar heel pain syndrome)
2. Distal plantar fasciitis (i.e. no heel pain, only arch pain)
3. Chronic plantar fasciosis

and possibly also include:

4. Plantar fascial pain due to partial ruptures of the CCPA.

Creation of a new term that included both the inflammatory, more acute condition of "plantar fasciitis" and the degenerative, more chronic condition of "plantar fasciosus", since we really never know how much inflammation vs degeneration is the cause of the pain in these patients, would make sense to me clinically.

What say all of you?

__________________
Sincerely,

Kevin

**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College

e-mail: kevinakirby@comcast.net

Private Practice:
107 Scripps Drive, Suite 200
Sacramento, CA 95825 USA
My location

Voice: (916) 925-8111 Fax: (916) 925-8136
**************************************************

Well I am good with this Kevin, but if we look at the pain generating condition as a 'syndrome', which personally I think it is, I believe this implies, as you rightly include, several conditions, with the possibility of more than one occurring simultaneously.
This being the case, I think we probably need to include the nerve involvement, which can be quite subtle and not necessarily produce overt neurological signs, but which I believe is quite often an important part of the symptomatology of chronic "plantar fascia stress syndrome", and may well be one of the reasons corticosteroid infiltration offers short term pain relief.
regards

S

One of the things I like about this forum is not feeling quite a odd a usual for being a nerd; what joy to share being animated about plantar heel pain :)

Anyhow Kevin's suggestion "Plantar fascia stress syndrome" sits well with me; I feel that the term syndrome generally implies a group of things which share a similar presentation, give the impression of some limited knowledge but in the spirit of Simon's prior post says to be candid

"we don't know"

what this about for sure

Simon what instrument do you play and is it a serious addiction?

Cheers

Martin


Foot and Ankle Clinic
1365 Grant Ave.
Winnipeg Manitoba R3M 1Z8
phone [204] 837 FOOT (3668)
fax [204] 774 9918
www.winnipegfootclinic.com

'73 360 Rickenbacher
"71 Gretsch Steven Stills reissue
American Standard Strat
97 Fender Tele
96 Fender Jagstang (the dirtiest guitar of al la k. cobain)
Gibson Les Paul Robot series one
Gretsch Chet Aitkins
1960 Gibson Les Paul Gold top reissue
Martin DC-16RGTE
Maton Lyrebird
Fender Telecoustic
Yamaha 'Silent Guitar'
Martin Classic collection
Ovation "performance'

according to my wife.. it is a serious addiction.. for me.. I need a '57 Strat amongst others and do not believe I have any issues at all..

Oh dear . .. . . these are mostly controlled instruments . . . plus denial you need help.

have you tried bagpipes or banjos? . . . . they are good for withdrawal . . . worked for me


Cheers

Martin

Simon:

After looking at that last list, I better get my vocal chords ready to rock n' roll.

Anyway, back to the classification of plantar fasciitis, I wouldn't recommend nerve involvement for this "plantar fascial stress syndrome" since I would consider these to be different pathologies (e.g. Baxter's neuritis, medial calcaneal neuritis, lateral calcaneal neuritis) and not specifically pathologies of the central component of the plantar aponeurosis.

Rather the purpose for the "plantar fascial stress syndrome" label would be to eliminate any reference to the inflammation of "fasciitis" and eliminate any reference to the degeneration of the "fasciosus" so that a syndrome that can include varying degrees of both inflammation and degeneration to the central component of the plantar aponeurosis could be better described, which, in all reality, is the true nature of the condition we all treat on a daily basis.

__________________
Sincerely,

Kevin

**************************************************
Kevin A. Kirby, DPM
Adjunct Associate Professor
Department of Applied Biomechanics
California School of Podiatric Medicine at Samuel Merritt College

e-mail: kevinakirby@comcast.net

Private Practice:
107 Scripps Drive, Suite 200
Sacramento, CA 95825 USA
My location

Voice: (916) 925-8111 Fax: (916) 925-8136
**************************************************

Effectiveness of Device-Assisted Ultrasound-Guided Steroid Injection for Treating Plantar Fasciitis
Chen, Chien-Min MD; Chen, Jenq-Shyong PhD; Tsai, Wen-Chung MD, PhD; Hsu, Hung-Chih MD; Chen, Kai-Hua MD; Lin, Chu-Hsu MD
American Journal of Physical Medicine & Rehabilitation, 6 December 2012

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