2. The term Navicular disease is used in this discussion to
denote a chronic progressive syndrome involving the
navicular bone, its fibro cartilaginous flexor surface, its
ligaments and capsular attachment, the deep digital flexor
tendon, and the navicular bursa.
Variable response to local analgesia of the medial and
lateral palmar digital nerve, the distal interphalangeal joint
space and the navicular bursa is noted. This variable
response suggests that sensory nerves innervating the
synovial membranes of the collatral sesamoidean ligament,
the distal sesamoidean ligament, distal sesamoidean impar
ligament, and the navicular bone itself play a separate or
combined role in mediating pain in navicular disease.
Because there is no proven cause or treatment it is better
referred to as a syndrome
Navicular Syndrome is generalized heel pain due to
problems with the navicular bone
Other causes of heel pain are often misdiagnosed as
Navicular Syndrome Dr2R Series
3. The navicular bone has
1- Flexor
1. Two surface
2- Articular
1- Proximal
2. Two border
2- Distal
1- Medial
3.Two extremities
2- Lateral
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4. It has two separate cartilage- covered articular
surface.
The larger proximal articular surface forms to the
condyles of the middle phalanx.
A smaller distal articular surface, associated with the
distal navicular border, is essentially a narrow facet
that articulates whit the distal phalanx.
The distal articular surface of the navicular bone and
the articular surface of the distal phalanx are usually
parallel but can be convergent.
The flexor surface has a prominent central ridge –
termed the central eminence.
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5. The deep digital flexor tendon and adjacent bursa
make contact with the fibrocartilage-covered flexor
surface.
The navicular bone is held in position by three
strong ligaments.
1- The paired suspensory ligaments originate from the
dorsolatral and dorsomedial aspects of the proximal
phalanx and attach to the praoximal navicular border
and both extremities.
2- The distal sesamoidan or impar ligament orginates
from projection on the disat navicular border just
coudal to the articular surface.
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7. Weight Bearing
Activates navicular bone
Compression of navicular bone Tension of supporting ligaments
Cartilage degeneration,
Especially on flexor surface
Abrasion of flexor
Tendon by eroded cartilage
Abnormal increase
In bone density
Navicular
Bursitis?
Fracture?
Navicular Syndrome
8. Weight Bearing
Activates navicular bone
Compression of navicular bone Tension of supporting ligaments
Ligament strain &
Inflammation, especially
At bottom
Reduced blood flow
To & from navicular
bone
Cavities (“flasks” or
“lollipops”) along lower edge
Loss of bone
Density around
vessels
Increased blood
Pressure within navicular
bone
Tearing of
Ligament(s)?
New bone
Production at
Sides (“canoeing”)
Compensation from
Vessels at upper edge
Navicular Syndrome
9. 1. Concussion or trauma to the Navicular bone
a Thinning and erosion of the cartilage
b Degeneration of the Navicular bone
c Injuries of the Navicular bone and surrounding
areas.
2. Arterial obstruction
* strain and inflammation of the impar ligament can
obstruct these blood vessels and reduce blood flow
to and from the navicular bone.
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10. interruption of the blood flow to and from the
navicular region has been proposed as
contributing factor in the development of
navicular syndrome. Thrombosis of navicular
arteries within the navicular bone , partial or
complete occlusion of digital arteries at the level
of the pastern and fetlock, and a reduction in the
distal arterial blood supply as a result of
atherosclerosis of the vessel, resulting in ischemia
were thought to be the cause of navicular
syndrome.
3. Changes in the Navicular bursa synovium
*Osteoarthrosis (degenerative joint disease)
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11. The syndrome has been shown to have a hereditary
predisposition, which is perhaps related to conformation.
Factor such as faulty conformation, hoof imbalance,
improper or irregular shoeing, and exercise on hard surface.
Poor hoof conformation
long toes and low heels
narrow upright feet
Extreme work on hard surfaces
Standing in stalls for extended periods of time
Improper trimming and shoeing
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12. Navicular syndrome is primary a slowly developing,
intermittent, bilateral forelimb lameness. It is also
occasionally recognized in the hindlimb.
In general, Navicular syndrome is most common
between 3 and 18 years of age(4 and 15 in adams),
with a peak incidence of 9 years of age at
presentation.
Males have involvement more often than do
females, gelding have a greater risk than stallion.
Often a unilateral lameness.
Usually restricted to the forelimbs.
Walking toe to heel.
Short choppy strides.
Reduced wear of the heel region.
The diagnosis is based on a characteristic gait, localization
of pain to the palmar part of the heel, identification of
radiographic signs of navicular degeneration ,and
elimination of other causes of lameness.
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13. Classically, it has been characterized as navicular
fibrocartiliginous degeneration whit secondary tendon
fibrillation.
Palmar cortex bone erosions can develop later. Other bony
changes involving the distal border synovial invagination
(enlargement) have also been noted.
Abnormalities such as dilated vessels, vascular thrombosis,
granulation tissue, and empty synovium-lined invagination have
been observed histologically to variable degree.
Enthesopathy involving the ligaments of the proximal and
distal borders can occur with or without distal border framina
changes.
Many of the gross and histologic features of navicular syndrome
support the concept of degenerative arthrosis.
Some evidence shows that chronic passive venous congestion of
the foot is related to navicular changes of elevated subchondrial
bone pressure and arterial hyperemia.
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14. Poor correlation of pathologic and radiographic finding
with clinical signs and prognosis has been demonstrated.
Horses without radiographic abnormalities may have
clinical navicular lameness, and horses with pathologic and
radiographic changes may be sound.
This paradox is explained in part by the fact that horses
have different thresholds, are subjected to wide ranges of
physical exercise, and are evaluated in variable stages of
disease.
Several authors agree that radiographic signs of navicular
disease in an otherwise clinically normal horses are
significant and may warrant prognosis for future
soundness.
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15. 1- Assessment of bony changes in Navicular Syndrome.
2- The identification of significant bone abnormalities
during prepurchase examination.
3- The assessment of bone or bursal involvement in
wounds or abscesses.
4- The evaluation of suspected trauma.
5- The collection of information about the
morphologic progression or remission of navicular
bone abnormalities.
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18. Navicular Bone
Standard views
Lateral and 45 degree DP (same
as for P3)
Horizontal DP (same as for P3)
65 degree DP Cone-down
Skyline (palmaroproximal
palmarodistal oblique)
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22. 2 methods (use grid with both)
Center on coronary band
Upright pedal
Cassette vertical
High coronary
Horse stands on cassette tunnel flat
on ground
Easier but more distortion
Tightly collimated to reduce scatter
and film fog
Navicular bone is superimposed on P2
Must not be superimposed on DIJ
Best view for evaluation of distal
navicular border
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23. Cassette in tunnel
X-ray beam angled along back of
distal pastern
Flexor surface
Corticomedullary distinction
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24. Proximal Border and Extremities
Enthesophytes (spurs) on the extremities
Remodeling.
Distal Border Changes
Synovial invaginations
Small osseous fragments
Flexor Cortex Changes
Cortical erosions
Mineralization of deep digital flexor tendon
Medullary Cavity Changes
Radiolucent cysts
Sclerosis
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26. Changes may be present
in sound horses
Distal border
Increased size and
number of synovial
invaginations
Cyst like lucencies
Entheseophytes
Collateral ligaments
(proximal border)
Impar ligament (distal
border)
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