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13 Biomechanics oftheDiabetic Foot: TheRoad toFoot Ulceration
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235
Fig. 13.2 (a) Spatiotemporal
data during GAIT (b) The
GAIT cycle and events
a
b
stress may occur at different anatomical sites of the diabetic
foot and may explain why some ulcers do not develop exclusively at high pressure locations [13, 14] (Fig.13.8).
A individual must be able to support or assume upright
position; maintain balance in an upright position during this
dynamic situation; initiate gait from a static (zero-speed
position) and control ambulation; develop new step forward;
generate muscular forces; anticipate the gravitational
forces; control the forces of momentum; and sustain and distribute the ground reaction forces (GRFs).
Changes intheFoot Caused by Diabetes
Diabetes mellitus affects the structure and function of the foot.
Many abnormalities which are a consequence of diabetes
including chronic sensorimotor neuropathy (DPN), foot defor-
mities, callus formation, limited joint mobility (LJM), high
plantar pressures, and autonomic dysfunction interact and contribute to the development of foot ulceration. In addition, diabetes affects the skin, tendons, muscles, and periarticular tissues.
Foot Deformities
Foot morphology, even without a specic pathology, determines the biomechanical behavior and functionality of the
foot. It is very important to consider both foot biomechanics
and morphology when planning a foot ofoading with
orthotics and/or special shoes, in order to reduce plantar
ulcer formation and thus avoid amputation in people with
diabetes [15].
Sensory neuropathy with loss of protective sensation
allows abnormal mechanical forces to cause painless injury
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P. V. Tsaklis and N. Tentolouris
to the skin or asymptomatic bone fracture [13, 16]. Motor
nerve involvement causes muscle weakness and atrophy with
foot imbalance leading to clawing of the toes, a high arched
foot or high pressure of the plantar surface [17, 18]. Muscular
atrophy has been dened as histological replacement of normal muscle by fat cells as a consequence of denervation [19].
Suzuki etal. found that neurogenic atrophy was associated
with fatty inltration of plantar muscles and impaired energy
metabolism in ulcerated [20]. In addition, foot deformities
are associated with and predictive of increased plantar pressures and foot ulceration [21, 22]. Prominent MTHs have
traditionally been attributed to weakness of the intrinsic
muscles of the foot leading to toe deformities [23]. Moreover,
fat cushions under MTHs which are imbedded in the exor
tendons are believed to migrate distally with clawing of the
toes, leaving the MTHs relatively unprotected [24]. Diabetic
neuropathic patients with a toe deformity have a greater
reduced sub-MTH padding compared with people without
this deformity, indicating increased probability of high pressure and risk for foot ulcer development at these sites [25].
Sensory neuropathy is often emphasized in considerations of
diabetic foot pathology; however, intrinsic muscle atrophy
does not necessarily appear to imply toe deformity, suggesting either that loss of foot muscles precedes the development
of toe deformities or that intrinsic muscle atrophy is not the
primary causative factor [25].
Charcot arthropathy causes gross deformation of the foot,
thereby affecting functional use of the foot and causing
abnormal pressure loading during walking. Peak plantar
pressure in patients with Charcot arthropathy over bony
prominences is higher compared with patients with a neuropathic ulcer [26]. People with minor amputations in the feet
exhibit abnormal pressure loading to the same and the contralateral foot [27]. Moreover, amputation of the hallux
greatly increases pressure under the MTHs [28, 29].
Increased plantar pressure is a strong risk factor for foot
ulceration [13, 30]. Beyond foot deformities, callus formation as discussed below has been associated with high plantar pressures and is highly predictive of foot ulceration [31]
(Fig.13.3).
Fig. 13.3 Orthotics design for ofoad and support during GAIT—case: left foot with Charcot arthropathy and right foot with amputation of the
2-3–4-5 rays
13 Biomechanics oftheDiabetic Foot: TheRoad toFoot Ulceration
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237
Thus, foot deformity as a consequence of DPN and callosities has been associated with abnormal foot loading during walking thereby causing high plantar foot pressures.
Alleviation of these high-pressure areas with accommodative footwear, including proper shoes and insoles, is necessary to reduce high pressures and to protect people with
diabetes from development of ulcers.
Sudomotor Dysfunction
Sudomotor dysfunction as a result of damage of the postganglionic sympathetic nerve bers (C-bers) that innervate
the sweat glands causes dryness of the skin of the feet. People
with diabetes who have a history of foot ulceration present a
high percentage of sudomotor dysfunction compared with the
diabetics with neuropathy but not foot ulcers and diabetics
without neuropathy [32]. Dryness of the skin of the feet can be
found in the vast majority of the diabetic patients with ulcers
compared to the diabetic patients without foot ulcers and can
cause ssure formation and in combination with increased
plantar pressure enhances callus formation [33]. Another consequence of the autonomic neuropathy is that it causes abnormal opening of arterio-venous shunting [34], which could
reduce capillary blood ow and impair oxygen delivery to the
tissues, consequently diminishing arterio- venous oxygen differences and impair skin oxygenation and wound healing [35].
Changes inTendon, Muscles, andBones
Several investigations have looked into changes in tendon
from diabetes. Plantar aponeurosis and exor hallucis longus
tendon are thicker in neuropathic patients as compared to
nondiabetic controls [36]. There is a trend of increased thickness of the plantar fascia and the Achilles tendon as diabetes
control worsens. These alterations result in changes in
ground reactive forces, force x time integrals, and equivalent
maximum loading times. Thus, for patients with foot ulcer,
the ground reactive forces are larger than the non-diabetes.
The equivalent maximum foot loading time is also higher in
all (vertical, anterior–posterior, and mediolateral) [37]. The
mechanical and metabolic muscle function is highly affected
from the impaired glucose regulation due to the dependency
on oxidative phosphorylation for energy production [38]. In
diabetes, the muscle strength reduces and thus leads to less
force in the calf and slower gait. Consequently the mis-ring
a reduction in neural pathways associated with muscle motor
units and ber types recruitment and deactivation will lead to
mobility alterations [39, 40]. As a result, mean plantar exion peak torque measured by an isokinetic dynamometer is
reduced in diabetes [41]. The ankle and knee muscle volume
and maximal isokinetic muscle strength are reduced in neu-
ropathic diabetic patients [42]. Thus, people with diabetes
and neuropathy exhibit delayed EMG responses, decreased
isokinetic muscle strength, and atrophy.
Muscle stiffness is a concept related to the previously
described changes in muscle weakness, atrophy, and tendon
thickening. Passive muscle stiffness relates to the resistance
of a muscle to elongation. When a neuropathic group examined muscle stiffness in relation to strength, range of motion
(ROM), and gait impairment, the researchers found that all
passive peak torque variables were associated with concentric peak torque, suggesting that intramuscular structures
contribute to both strength and stiffness [43, 44]. The neuropathic patient also uses passive torque for a larger proportion
of total torque output. There is a substantial decrease in concentric plantar exor peak torque, which may lead to instability when the center of mass passes anterior to the ankle
joint, but there is no signicant correlation between passive
stiffness and ROM [44]. Thus, the muscle strength and sensation may be more related to dorsiexion at the ankle [43].
Compared to non-DPN diabetic patients, the passive stiffness is not different. Data suggest that passive stiffness
explains a signicant amount of variance in walking speed.
This may have clinical bearing in brace use in this population
to increase passive stiffness [45].
Dynamic EMG research reported that the tibialis anterior
muscle which is responsible to control eccentrically the attening of the foot after the heel–strike phase remained active
for a longer duration of time in DPN patients compared to
healthy controls [39]. The vastus lateralis muscle lags during
walking and thus develops increased loads during heel–strike,
followed by a shorter duration of activity of the lateral gastrocnemius. An early activation of the triceps sural muscle
leads eventually the forefoot and more anterior regions of the
foot to make an early contact with the ground surface [39].
Under these circumstances, the temporal progression of
the plantar surface and contact to the oor during stance, from
the heel to the metatarsal heads and hallux, follows an abnormal route and propulsion. Consequently, high peak pressures
occur on the anterior plantar areas at the initial heel contact
due to its premature contact and will be added and accumulated to the forefoot that will bear loads during the toe-off
phase which follows. This prolonged overload throughout the
foot rollover process (at early and late stance), associated
with the reduced sensitivity, would increase the risk of tissue
breakdown in the diabetic neuropathic foot [39].
Data regarding the effect of diabetes on bones are contradictory. In the Women’s Health Initiative Observational
Study, it was found higher hip and spine bone mineral density in postmenopausal women with diabetes in comparison
with non-diabetic women [46]. A small study described
lower bone mineral density in the calcaneous of patients with
diabetic neuropathy and in diabetic patients with mid foot
deformity in comparison with nondiabetic individuals [47].
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Limited Joint Mobility
The factors limiting ankle joint dorsiexion are anatomical,
physiological or orthopedic in the non-diabetic population,
but in diabetic individuals, glycosylation may be an important factor in altering the joint motion. There is a linear relation between diabetes and foot morphology decits,
especially in the presence of neuropathy.
Chronic increased tissues exposure to hyperglycemia
alters their composition and functionality. Non-enzymatic
irreversible glycosylation of proteins and formation of
advanced glycosylation end products (AGEs) alters the
mechanical properties of tissues and typically causes reduction in elasticity [48, 49]. The skin of the diabetic patients is
thicker and less elastic in comparison with that of healthy
people [50, 51]. Collagen bundles in the dermis of people
with diabetes are thickened and disorganized as a result of
irreversible glycosylation of collagen. Collagen has a low
turnover rate, and the formation of AGEs damages the protein itself and reduces the ability of collagenase to remodel
the collagen bers [48]. One study found that the keratin in
the stratum corneum of the diabetic foot was glycosylated
compared with nondiabetic skin [52]. This may impair the
capacity of the skin for the distribution of pressure.
A further consequence of AGEs formation is the limitation of range of movement in many joints of the body in
people with diabetes [20]. Regarding etiology of LJM, most
evidence suggest a relationship with the collagen abnormalities and nonenzymatic glycation of soft tissue that occurs in
diabetes, resulting in thickening of tendons, ligaments, and
joint capsules, thereby reducing tissue exibility [48, 53–
55]. LJM has been described rst in the hand and can be
easily demonstrated by inability to atten the hand on a table
top or by failure to approximate the palms with the ngers
fanned and the wrist maximally exed (prayer sign) [53].
The prevalence of LJM (diagnosed with a positive “prayer
sign”) has been reported to vary between 49% and 58% for
type 1 diabetic patients and between 45% and 52% for
patients with type 2 [55–57].
The rst metatarsophalangeal joint (MTPJ), acts as a
powerful second type lever during the body propulsion at the
toe-off phase of gait. In people with DPN, appears substantial biomechanical dysfunction, leading to elevated plantar
pressures during gait [39]. Ulceration under the great toe has
been constantly associated to a reduced ROM at the rst
MTPJ [8]. Patients with a history of rst MTH ulceration
have signicantly diminished ability for dorsiexion at the
rst MTPJ and at the same time increased peak plantar pressure under the rst MTH; LJM of the rst ray explained
almost 50% of the variance in peak rst MTH plantar pressure [8].
Limited joint mobility is associated with abnormally high
plantar foot pressures and can contribute to foot ulceration in
diabetic patients who have neuropathy [58]. Veves etal. found
reduced subtalar joint mobility and increased foot pressures
in people with diabetes, compared to nondiabetic controls
and that diabetic Caucasians had reduced joint mobility and
higher plantar pressures in comparison with diabetic African
Americans, suggesting that there are racial differences in
joint mobility affecting foot pressures [59]. There is a signicant relation between LJM at the subtalar and ankle joint and
increased foot pressures in people with diabetes [60]. The
maximum movements at the ankle are delayed and slowed in
people with long-standing type 1 diabetes and the ROM is
linearly associate with the severity of the diabetic neuropathy
[61]. In the case of diabetic patients with ulcers, there is a
signicant impairment in the ROM of the subtalar joint in
comparison with non-diabetic controls and diabetic patients
without ulcers [62]. In addition, type 1 diabetic people in
India were found to have LJM of the foot which decreased
further with longer duration of diabetes [63].
The passive and active range of motion at the ankle and
rst MTP joint was assessed in a cross-sectional study including people with diabetes, with diabetic neuropathy, with foot
ulcer, and a nondiabetes reference group. The authors found
signicant reductions in both measures for rst MTP joint
dorsiexion for the ulcer group vs. the reference group. [64].
There might be associations between neurologic indices and
forefoot deformity as well as limited mobility of the rst
MTP joint in people with type 2 diabetes [65]. Comparing
people with type 1 and type 2 diabetes as well as healthy controls, there is a reduced joint mobility at the ankle and the rst
MTP joints in patients at high risk for foot ulceration as compared to those with diabetes not at high risk and the controls.
In those cases, the pressure-time integrals are signicantly
higher in the foot-at-risk patients compared with the others
and there is a strong inverse correlation between the mobility
of the ankle or rst MTP joints and the pressure-time integrals of the diabetic patients [66].
Another factor which inuence is aging. Aging and diabetes cause a signicant reduction in the plantar and dorsal
exion of foot ankle joint mobility, though after adjusting for
age, diabetes specically reduces plantar exion only [67].
The rst ulceration can be signicantly detected on the
foot which presents lower ankle joint mobility and eventually, the ankle joint mobility remains lower in patients with
history of previous foot ulcer [67].
There are limited data on the effect of interventions aiming
at improvement of ROM in people with diabetes and no data
on the association with foot ulceration. Passive physical therapy in patients with foot ulceration can improve joint mobility
and reduce plantar pressures [68]. More active exercise therapy must focus on the improvement of joint mobility, muscular performance, and walking speed in diabetic patients [69].
Foot ulcers are frequently healed using casts for offloading and in addition patients are advised to minimize their
13 Biomechanics oftheDiabetic Foot: TheRoad toFoot Ulceration
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239
level of physical activity while healing the ulcer; these two
factors may compromise joint mobility. The use of
N-phenacylthiazolium bromide, a substance that cleaves collagen crosslinks, could help in combination with passive
mobilization, to improve joint mobility. [70, 71].
People with diabetes develop changes in weight bearing
during ambulation, due to limited joint mobility that occurs
mostly at metatarsophalangeals and subtalar joints. The
transfer requires postural adjustments and is crucial to facilitate the walking as well as to maintain the balance during
dynamic tasks. The weight distribution between the lower
limbs (weight shift) is an important parameter and can be
measured in a quite bipedal stance, using force and pressure
platforms (Fig. 12.5). Patients with DPN have uneven weight
distribution in each leg, especially in the presence or history
of ulcers. The uneven weight distribution is notable when the
difference between the legs exceeds the 5–8%. In this case,
there are usually anatomical differences, like the leg length
that may required a customized foot orthotic. In the case of
no leg length difference, other functional reasons, such as
affected trunk alignment (e.g., scoliosis), weakness of gluteus medius, pelvic and core musculature shortening and/or
weakness, hip joint capsule and ligaments stiffness, morphological differences between the feet (like the high of the foot
arch) may be the main cause.
The active and passive range of motion (ROM) of the
main foot joints, which act dynamically during the stance
phase of gait, such as the rst metatarsophalangeal joint (rst
MTPJ) and the ankle and subtalar joints, can be measured
using special goniometers (hand held or digital) (Fig.13.4).
In summary, diabetes may exacerbate reduced joint
mobility that typically occurs with aging and many studies
found an association with the severity of diabetic neuropathy
and previous foot ulceration. However, it is important to note
that most of the evidence on the relationship between LJM
with foot ulceration came from cross-sectional studies. There
is need for prospective studies to examine the relationship
between LJM with foot ulceration as well as to examine
whether interventions aiming at increased joint mobility
affect incidence of foot ulceration.
Fig. 13.4 Range of motion measurements with a goniometer, for the ankle—subtalar and rst metatarsophalangeal joints
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Fat Pad andPlantar Fascia Changes
Many studies described atrophy, relocation, and changes in
absorption and shear properties in fat pads for people with
diabetes [72, 73]. Nondiabetic people in comparison with
diabetic patients with and without ulcers have thicker fat
pads at the heel and rst and second metatarsal heads in [74].
The submetatarsal fat pads appear signicantly thinner and
the subphalangeal fat pads signicantly thicker in the neuropathic patients with deformity compared with neuropathic
control patients, suggesting thinning and distal displacement
of the fat pad due to the contracture of the digits [73]. The
reduced fat pad is associated with bony deformity and
increased peak plantar pressures [74]. Rheumatoid arthritis
and diabetes can cause foot deformities, reduced fat pad, and
abnormally high pressures under the feet. In people with diabetic neuropathy and in people with rheumatoid arthritis
with similar foot deformities, plantar pressures are evenly
high, but only the diabetic patients with neuropathy develop
foot ulcers [74]. This emphasizes the importance of the loss
of sensory awareness in the pathogenesis of diabetic foot
ulceration, and suggests that high pressure alone is not a
direct cause of ulceration [75]. Reduction in fat pad can be so
prominent in some patients with claw toe deformity that the
condyles of the MTH can be palpated under the skin. In addition, callus can develop at the tips of the clawed toes due to
the high concentrated pressure.
Plantar fascia is a critical element in the transmission of
force through the toes. The diabetic patients present increased
thickness of plantar fascia. Thus, in association with the
mobility of the MTP joint and the forces expressed under the
metatarsal heads, the patients with foot ulcers compared with
non-diabetic have a signicantly reduced ROM at the MTP
joint and increased vertical and mediolateral forces [76].
Limited evidence suggests that rupture of the plantar fascia
after repetitive chronic stress can contribute to the development of toe deformities [77].
These data suggest that fat pad is reduced in diabetic
patients with neuropathy and foot deformities and it is associated with increased plantar pressures. The thickness of the
plantar fascia is increased in people with diabetes and it is
associated with reduced ROM and high plantar pressures.
High Plantar Pressures
As described before, a number of foot alterations in people
with diabetes cause increased plantar pressures. Early observations described that most neuropathic ulcers occur on the
toes (39%), the hallux (30%) and the metatarsal heads (24%)
[78]. These areas are of principal concern in understanding
the causes of elevated pressure. Veves etal. described that a
value of over 1000kPa during barefoot walking is required
for the development of an ulcer over a 2.5 year follow-up
period; in contrast no ulcer developed in patients with lower
plantar pressures. These ulcers developed in high pressure
areas like the MTH [13]. A threshold of 700kPa has a high
percentage sensitivity and specicity for the prediction of
foot ulceration [79] and peak pressures over 875kPa seem
capable for prediction of foot ulcer development [80].
The isolated measure of peak pressure does not incorporate a time dimension. It is important to examine the role of
pressure time integral and plantar stress in the development
of ulcer. Diabetic patients with neuropathy and ulcers have
higher peak forefoot pressures and pressure time integrals
than diabetic patients without neuropathy [81].
Patients with recurrent ulcers are less active and compile
less daily stress, expressed as the product of mean daily
strides and forefoot pressure-time integral, than diabetics
without neuropathy and non-diabetic controls. The patients
with a history of ulcer may be more susceptible to plantar
tissue injury even at relatively low levels of activity and
cumulative tissue stress [82]. Although individuals with diabetes who develop ulceration have a lower overall activity
than their counterparts with no ulceration, activity levels in
ulcerated patients have a high degree of variation, which
increases further a few weeks prior to ulceration [83].
Barefoot walking is believed to be a principal cause of
foot ulceration. Some patients may protect their feet adequately in footwear throughout the day, yet ulcerate because
of barefoot walking at home [9]. The type of shoes worn is
important; thus, walking in shoes with leather soles is almost
equivalent to walking barefoot while walking in simple sport
shoes (trainers) can reduce pressure up to 50% [9]. Pressure
reduction strategies alone do not have the greatest impact on
preventing reulceration. Τherapeutic footwear and orthotic
devices reduce drastically (by 50-80%) plantar pressures but
many (26-42%) of these patients reulcerate within
12–18months [84, 85]. Observational studies have shown
that only 22–29% of individuals wear their prescription footwear for 80% of the daytime [86]. Patients who adhered to
wearing custom-made footwear are less likely to reulcerate
in a mean follow-up period of 18months [87]. It is believed
that people with diabetes view their homes as safe zones and
may not wear the prescribed footwear, despite taking over
50% of the daily steps at home [9]. An additional factor that
affects compliance is the perceived benet of the footwear in
prevention of foot ulcer [88].
Another important issue is the contribution of pressure
gradient in the pathogenesis of foot ulcers. Pressure gradient
is dened as the spatial change in plantar pressure around the
peak pressure location. The mean peak pressure gradients
develop higher in the forefoot than in the rearfoot, whereas
the mean peak plantar pressure is only 36% higher in the
13 Biomechanics oftheDiabetic Foot: TheRoad toFoot Ulceration
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forefoot than in the rearfoot. Moreover, the peak pressure
gradient forefoot-to-rearfoot ratio is nearly two times greater
than the peak plantar pressure forefoot-to-rearfoot ratio.
Thus, the peak pressure gradient appears to provide additional information about the stresses experienced by the soft
tissues of the foot, especially in the forefoot [89]. Additionally,
the maximal shear stress is by 1.29 times higher and closer to
the surface in the forefoot compared to the rearfoot, with signicant correlations between maximal shear stress and peak
pressure as well as maximum pressure gradient [90].
Charcot foot with a “rocker bottom” deformity is associated with increased plantar pressure [91]. Many persons with
this deformity develop recurrent ulcers over the bony prominences. The deformities associated with Charcot affecting
less commonly the ankle or rearfoot are often multiplanar,
resulting in sagittal, frontal, and rotational malalignment
[92]. In addition, shortening of the limb often occurs from
collapse of the distal tibia, talus, and calcaneus [93]. These
deformities also result in alterations in the biomechanics of
the foot. For example, a varus ankle or rearfoot results in
increased lateral column plantar pressure of the foot, predisposing the patient to lateral foot ulceration. Collapse of the
talus, secondary to avascular necrosis or neuropathic fracture, further accentuates these deformities and contributes to
a limb-length inequality [93].
241
Recording andEvaluation ofthePressures
around thePlantar Area
Plantar pressure measurement is being used in both research
and clinical practice to compare gait patterns of different
clinical groups and to evaluate the effect of footwear,
orthotic, and surgical interventions [94].
When someone stands upright and much more when
ambulates or run, the foot structures receive high pressures.
As pressure is dened as the quotient of the force (including
weight and muscle force) exerted on the foot by a surface
that receives this power. The pressure is expressed in kg/cm2
or in kPa (kilopascals). Since a typical man’s size −10 foot
has a total area of approximately 130cm2, the average pressure under the foot is of a 100-kg person would be 0.77kg/
cm2 or approximately 75 kPa. It is estimated that plantar
pressure is by 40% greater during running than those encountered during walking. Moreover, the pressure that applies on
tissues during walking under a callus or a scar from a healed
ulcer can be almost 10–15 times higher compared to healthy
people [9].
Pedobarographic Evaluation
For the recording and the evaluation of the plantar pressure
distribution, there are in the market special platform like
apparatus (pedobarographs or FPPs), which consist of digital
Fig. 13.5 Static and dynamic measurements using a foot pressure platform (pedobarograph); static measurement data: Pressure distribution
around the plantar area; center of pressure (COP) orientation on the
transverse plane; The body weight % distribution between the legs
(weight shift); COP kinetic data (COP sway velocity and area)—
dynamic measurement data: Pressure distribution around the plantar
area during the stance phase of GAIT; COP route from heel strike to
toe-off
sensors and calculate the force per square area (N/cm2) (pressure in KPa). The amplitudes of the applying forces attributed analogously through a RGB color scale (with the highest
pressures draw red and the lowest draw blue). As a result, a
full image of the loading plantar area of the foot can be
acquired, with the specic coloration based on the recorded
pressures (Fig.13.5). For the pressure distribution, the subject adapts an upright standing (static) position (usually a
quite bipedal stance), barefoot for some seconds.
Most Common Foot Deformities andHigh Risk
Pressure Distribution
The foot structure is dominant in predicting peak pressure
[13, 26] (Fig.13.6).
A foot can be characterized as cavus if the middle third of
the footprint cover less than the 2/third of the forefoot print’s
width; planus (at) if the width of the middle third of the
footprint exceeds 1/third of the full foot width. The heel
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Fig. 13.6 Pressure distribution on the foot plantar area; The ve segments we can divide the foot plantar area using Bowen’s model, MF medial-
forefoot; MM medial-midfoot, LF lateral-forefoot, LM lateral-midfoot and heel
deviation (eversion—inversion) can be evaluated by comparing the Helbing line (drawn along the Achilles tendon) with
the vertical one. A valgus deviation higher than 38° is considered as a valgus heel (eversion—peak pressures locate at
the medial aspect of the heel). A varus deviation is considered as a varus heel (inversion—peak pressures locate at the
lateral aspect of the heel) [15]. Additionally, a Hallux valgus
is dened as a deviation of the great toe toward the lateral
side of the foot with a prominence developed over the medial
side of the rst metatarsal head. In this case, the COP route
during the rollover process is highly affected and lead to an
overload of the lateral metatarsals and also instability during
the toe-off phase of gate [15] (Fig.13.7).
In the case of cavus diabetic foot, there are higher peak
and mean peak pressure values on the forefoot area, when
compared with people with normal foot. This phenomenon
has also been related to submetatarsal pad displacement and/
or increased stiffness in non-DPN and DPN patients, as well
[15, 95].
In case of abnormal alignment of the foot with an uncompensated forefoot varus or forefoot valgus (inverted or
everted forefoot), high pressures appear located at the rst or
fth metatarsal head respectively. For the same dynamic reasons, an inverted heel and load is associated with lateral heel
high pressures, whereas an everted heel position gives medial
heel high pressures [96].
13 Biomechanics oftheDiabetic Foot: TheRoad toFoot Ulceration
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Fig. 13.7 Case: Hallux
valgus, static and dynamic
measurements. Weight
shifting on the normal side. A
prominence developed over
the medial side of the rst
metatarsal head. Overload of
the lateral metatarsals and
instability during the toe-off
phase of GAIT
243
The Spatiotemporal—and Kinetic Parameters
During Ambulation
The spatiotemporal parameters are reduced in DPN patients
compared to non-DPN diabetic and healthy people. The
DPN-related changes in the lower limbs lead to gait variations and decits; individuals with DPN walk slower than
healthy people and have smaller stride length. Studies
reported also, slower walking speeds in the DPN patients
compared to non-DPN patients, with a longer percentage
duration in the stance phase of gait and a longer stance time
[39]. One hypothesis is based on the dynamics of the kinematic chain of the limb, where the force generation at the
hip, knee, and ankle increase signicantly for both exion
and extension moments in patients with DPN [39]. The
excess of hip exion is also another compensatory mechanism to increase stability in the gait strategy of DPN patients,
adjusting the impaired ankle dorsiexion [39].
Kinetics oftheDiabetic Foot During Gait
The forces generate during heel strike and toe-off phase of
gate in patients with DPN have lower magnitude compare to
non-DPN diabetics and healthy people [97]. The rst maximum support moment (combination of extensor moments at
hip, knee, and ankle) and the mid stance minimal support
moment appear elevated in DPNs compared with non-DPN
diabetics (this suggests that combined forces at the hip, knee,
and ankle during the stance phase are greater in DPN patients
compared to the others); however, the second maximum support moment seems slightly higher in the Non-DPN diabetic
patients when compared to DPN patients [97, 98]. Additionally,
people with DPN generate greater knee exion moment compared to non-DPN diabetic and healthy people [97], probably
because knee exion might be an important compensation
strategy in those with DPN, as the motor component of DPN
manifests in a stocking and glove distribution and affects the
distal joints rst [39]. They also generate greater hip extension
moment and reduced hip exion moment [98].
The ground reaction force (GRF, Z-axis) during the initial
contact (heel strike) and in some cases during toe-off are
higher in DPN patients compared to both non-DPN diabetic
and healthy people due to the neurological decit and
reduced proprioception [39]. The forward peak and backward peak of the anteroposterior ground reaction force
(Y-axis) component appear reduced during the stance phase.
DPNs with previous neuropathetic ulcer showed a signicant
increase of the mediolateral stress (X-axis), especially under
the metatarsals [94] (Fig.13.8).
In the presence of ulcers or ulcers history on the foot,
DPN patients would continue to demonstrate similar abnormal lower limb biomechanical characteristics, like reduced
spatio-temporal parameters such as speed of walking and
stride length, restricted kinematics, delayed muscle activations, and altered forces (kinetics), which may contribute to
elevated plantar pressures during gait and entrap the person
into a vicious cycle of repetitive pathology [99].
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Fig. 13.8 Ground reaction
forces during the stance
phase; Case: vertical GRF
(Z-axis) differences between a
diabetic neuropathic and a
non-diabetic stance phase; (a)
heel load, (b) midfoot load,
(c) forefoot load and (d)
phalanges load. During the
diabetic stance, the midfoot
load (b) is reduced and short
timed and thus we observe a
quick transition and overload
on the forefoot
P. V. Tsaklis and N. Tentolouris
Concisely, the four biomechanical diversications for
patients with DPN compared with the normal gait are abnormal spatio-temporal outputs, such as speed of walking and
stride length; restricted kinematics (movement patterns);
altered kinetics, (altered forces); and elevated plantar pressures on the ulcerated and non-ulcerated foot.
Plantar Callus
Plantar callus develops mainly at areas of high vertical pressures like the MTH and hallux [100]. Callus acts as a foreign
body and acts to elevate further pressure resulting in positive
feedback for the production of callus. Callus, if left, results
in injury to the underlying tissues in the presence of loss of
protective sensation [100], while its removal reduces plantar
pressure and prevents ulcers [101]. Delbridge et al. suggested that the initial event in the formation of a neuropathic
plantar ulcer is the development of callus [102]. Then tissue
injury occurs under the callus and a cavity is formed that is
lled with blood (hemorrhagic callus or pre-ulcer). This cavity enlarges with further walking until it causes a rupture of
the skin surface forming an ulcer. Prospective data demonstrated that the presence of plantar callus was highly predic-
tive of subsequent ulceration and callus is recognized as a
“high risk” factor for foot ulceration [103].
Previous Foot Ulceration
Previous ulceration is a leading risk factor for future ulceration. In addition to the risk factors, a patient has to develop
the rst ulcer; altered mechanical properties of the new tissue generated during wound healing may increase further the
risk [104]. Actually, little is known about the properties of
tissue formation during wound repair [105]. It is believed
that the hard scar tissue that is formed may act in much the
same way that callus act by transferring increased pressure to
the underlying soft tissues. Indeed, Murray et al. demonstrated that a history of previous ulceration offered the highest relative risk (56.8) for reulceration compared to a much
lower relative risk (11.0) for an ulcer developing under an
area of callus [31]. Contrary to what was previously thought,
patients with active ulcers have reduced plantar pressure
compared to those with DPN without ulcers, probably
because they adapt a more “conservative and consciously
depended gait strategy.” Of course, that will eventually affect
and overload the contralateral foot (Fig.13.9).
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