Mel,

I wrote:
> << The plantar fascia provides supination moment to the foot via the
windlass
> mechanism. In the presence of excessive STJ pronation moment the loading
on
> the plantar fascia may be increased, leading to micro-failure at the
> enthesis.  We examine spatial orientation of the STJ axis and the position
of
> the CoP relative to this. By providing an external source of supination
> moment either via orthotics or taping (although the ability to do this
with
> tape is highly questionable) we may "off-load" the plantar fascia to some
> degree. >>
>

You replied:
> *** Please give some more details of the degree to which the
non-contractile,
> non force-producing fascia provide a moment by acting like a pulley,
> especially since a moment is defined as the product of a force and the
> perpendicular distance from the fulcrum to the line of action of the
force?

The windlass mechanism of the plantar fascia was first described by Hicks in
1954 (Hicks, J.H.: The mechanics of the foot. II. The plantar aponeurosis
and the arch. J. Anat 88:25, 1954). The central band of the plantar fascia
arises from the medial tubercle of the calcaneus and passes distally to
insert into the base of the phalanges of all of the toes. As the toes are
brought into dorsiflexion, the plantar fascia is wrapped around the
metatarsal heads (variation in diameter of each metatarsal head results in a
geared mechanism such that tension in each individual slip is a function of
the degree of digital dorsiflexion and the sagittal plane diameter of each
metatarsal head) this in turn causes elavation of the medial longitudinal
arch and a supination moment at the subtalar joint since the origin of the
plantar fascia lies medial to the STJ axis at a perpendicular distance to
it.

> Is this moment large enough over a few degrees of increased pronation to
> cause adequate strain in the fasciae? Has this action been shown to cause
> "microfailure" or is this only an hypothesis so far?

Interesting question, while this has been assumed, to the best of my
knowledge this has not been demonstrated either clinically or in vitro. Like
the majority of studies re: aetiology of musculoskeletal disorders, research
tends to be correlational :-(

>Only muscles or
> external forces may produce moments and it is not the muscles, so that the
> postulated moment must be the result of external movement as encountered
> during stabilisation or gait.

Your above conjecture is just not true- sorry. Any tissue which generates a
force about a joint axis may produce moment- simple physics.

Here's one hypothesis: With increasing pronation the STJ axis moves
medially, this provides reduced contact area on the plantar foot for GRF to
act to provide external supination moment. During gait, the STJ  pronates at
heel strike (since net moment = pronatory) and then begins to resupinate
just before midstance, thus we must move from a net pronation moment to a
net supination moment for this to occur; since pronation has been
decelerated, stopped and reversed during this time. Where is the supination
moment generated to decelerate the pronation? There are several
possibilities, including externally: CoP medial to STJ axis. If the CoP lies
lateral to the STJ axis it will produce further pronation moment. The
internal structures which can provide supination moment may be roughly
broken down by tissue type:  Muscle: any muscle inserting medially to the
STJ axis at this time, e.g. post tib/ gastroc/ soleus; Ligament: spring
ligament, plantar fascia; Bone: the floor of the sinus tarsi. The key is
with increasing pronation moment and /or pronated position of the STJ, the
structures which can supply supinatory moment are put under increasing
demand in order that pronation be decelerated. Clinically, we see patients
presenting with sympoms relating to these overuse in these structures
concomittantly with medially deviated STJ axes/ "excessive" pronation during
gait viz a viz posterior tibialis dysfunction, plantar fasciitis / spring
ligament degeneration, sinus tarsi syndrome - OK there is a big cause and
effect deal to work out here, but we can model this mechanism of
pathogenesis pretty satisfactorially using free-body analyses and inverse
dynamics. What we don't know is why some people show pathology in one
structure rather than another, this is likely to be where genetics has a big
role, but it is evident (and obvious) from both a modelling and clinical
perspective that those with sinus tarsi pathology are maximally pronated at
the STJ.

For more info on all of this see:
Bojsen-Moller, F. Lamoreux, L.(1979): Significance of free dorsiflexion of
the toes. Acta orthop. Scand. 50 471-479
Dananberg, H.J. (1993): Gait style as an etiology to chronic postural pain
part 1. JAPMA, 83(8) 433-441
Dananberg, H.J. (1993): Gait style as an etiology to chronic postural pain
part 2. JAPMA, 83(11) 615-624
Dananberg, H.J. (1999): Chronic low back pain & its response to custom-made
foot orthoses. JAPMA, 89(3) 109-117
Dananberg, H.J. (2000): Sagittal plane biomechanics. JAPMA 90(1) 47-50
Fuller, E.A. (1999): Center of pressure & its theoretical relationship to
foot pathology. JAPMA, 89(6) 278-291
Fuller, E.A. (2000): The windlass mechanism of the foot. JAPMA, 90(1) 35-46
Kirby, K.A. (1987): Methods for determination of positional variation in the
subtalar joint axis. JAPMA, 77(5) 228-234
Kirby, K.A. (1989): Rotational equilibrium across the subtalar joint axis.
JAPMA, 79(1) 1-14
Kirby, K.A. (2000): Biomechanics of the normal and abnormal foot.JAPMA,
90(1) 30-34
Nester, C.J. (1998): Review of the literature on the axis of rotation at the
subtalar joint. The Foot, 8(3) 111-118
McPoil, T.G., Hunt, G.C. (1995): Evaluation & management of foot & ankle
disorders: present problems & future directions. JOSPT, 21(6) 381-388

> <<Also recent research shows a direct relationship between tension in the
> plantar fascia and tension in the Achilles tendon and degree of
dorsiflexion
> at the hallux: stretch soleus /gastroc with toes dorsiflexed.  >>
>
> *** Did this research conclude that this relationship was correlative or
> causal?

Don't have the paper to hand so I'll need to get back to you on this. As I
recall, it was done in vitro using increasing force applied to the tendon
via a jig and varying degrees of dorsiflexion at the hallux and lesser toes.

Hope this helps.

Best wishes,
Simon
**************************************************
Simon K. Spooner PhD, BSc, SRCh
Lecturer Biomechanics
Plymouth School of Podiatry
North Road West
Plymouth, UK
PL1 5BY
*************************************************