Tutorial Article - AAEP · development of navicular disease (Dik et al.2001a,b). Finnhorses and Friesian horses tend to have a straight or convex contour of the proximal articular

Tutorial Article Current concepts of navicular diseaseS. DYSON*, R. MURRAY, T. BLUNDEN† AND M. SCHRAMME‡

Centre for Equine Studies and †Centre for Preventive Medicine, Animal Health Trust, Lanwades Park, Kentford,Newmarket, Suffolk CB8 7UU, UK.

Keywords: horse; navicular disease; lameness.

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What is navicular disease?

Navicular disease is a chronic forelimb lameness associatedwith pain arising from the distal sesamoid or navicular bone. Itis well recognised that in association with advanced naviculardisease, fibrillation of the dorsal aspect of the deep digitalflexor tendon (DDFT), with or without adhesion formationbetween the tendon and the navicular bone, are commonfeatures (Figs 1 and 2). Recent clinical studies using magneticresonance imaging (MRI) (Dyson et al. 2005) and post mortemstudies (Blunden et al. 2006a,b) have demonstrated that theremay also be abnormalities of closely related structures,including the collateral sesamoidean ligaments (CSLs), distalsesamoidean impar ligament (DSIL) and navicular bursa. Forthe purposes of this article this complex of degenerativechanges will be referred to as navicular disease. Primary injuryof the DDFT is considered to be a separate condition (Dyson etal. 2003), which may have a different aetiopathogenesis.

Although historically considered to be a single disease,given the variety of clinical presentations it is likely that thereare a number of different clinical conditions, of differentaetiologies, that give rise to pain in the navicular apparatus. Itis difficult to conceive of a single disease which can result inan insidious onset, slowly progressive bilateral forelimblameness, or an acute onset, relatively severe unilateralforelimb lameness, each with a variety of different radiologicalmanifestations and with some horses never developingradiological changes. It is curious that sometimes clinical signsbecome apparent in young horses just commencing work,whereas more typically lameness is seen in mature ridinghorses. It is also seen in horses with vastly different distal limbconformation. It is a common condition in Quarter Horses,which tend to have narrow, upright, boxy feet, small relativeto their body size, as well as in European Warmblood horses,many of which have relatively tall narrow feet. It is alsocommon in Thoroughbred horses, which frequently have

*Author to whom correspondence should be addressed. ‡Presentaddress: Department of Clinical Sciences, College of VeterinaryMedicine, North Carolina State University, 4700 Hillsborough Street,Raleigh, North Carolina 27606, USA.

Fig 1a: Left front navicular bone of a horse with advanced end-stage navicular disease. There is major loss of fibrocartilagefrom the entire flexor aspect of the navicular bone, withexposure of subchondral bone. There are central and distaladhesions of the deep digital flexor tendon.

Fig 1b: A navicular bone with widespread thinning of thefibrocartilage; there is a depression into the subchondral bonelateral to the sagittal ridge, to which the deep digital flexortendon was adherent.

Fig 1c: A navicular bone with partial-thickness loss offibrocartilage axially in the distal third of the bone. There wereadhesions of the deep digital flexor tendon in this area.

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rather flat feet with low collapsed heels, often associated withdorsopalmar foot imbalance (Fig 3). Evidence has recentlybeen presented suggesting that there is a heritable tendencytowards the development of navicular disease in Dutch andHanoverian Warmblood horses (Dik and van den Broek 1995;Dik et al. 2001a; Stock et al. 2004).

The factors causing pain in the navicular apparatus, andtherefore lameness, are poorly understood. Experience withboth radiography and MRI suggests that lesions in both thenavicular bone and closely related structures are likely topredate the onset of lameness in some horses (S. Dyson et al.,unpublished data). In some horses, a trigger factor apparentlypromoting pain and lameness has been a period of enforcedrest for an unrelated cause.

There have been no good epidemiological studiesinvestigating risk factors for the development of naviculardisease. Information is therefore largely anecdotal. Thefrequency of occurrence of navicular disease appears to varybetween breeds. Quarter Horses (Ackerman et al. 1997),Warmblood horses (Mey et al. 1967) and Thoroughbred-crosshorses (Colles 1987) have a relatively high incidence, whereasthe occurrence and/or recognition in some breeds such as theFinnhorse, Arab (Turner 1993) and Friesian is relatively low.

Biomechanical considerations

The navicular apparatus comprises the navicular bone, CSLs,DSIL, navicular bursa, DDFT and distal digital annular ligament.The navicular bone, which articulates with the middle anddistal phalanges, provides a constant angle of insertion andmaintains the mechanical advantage of the DDFT, which exertsmajor compressive forces on the distal one third of the bone.Contact studies between the phalanges in isolated limbs havedemonstrated that the greatest forces are applied in thepropulsion phase of the stride. This occurs during extension ofthe distal interphalangeal (DIP) joint, with increased pressureof the DDFT on the palmar aspect of the navicular bone,increased contact between the navicular bone and the middlephalanx and increased tension in the CSLs (Denoix 1999a;Bowker et al. 2001; Wilson et al. 2001). Tension in the DDFTand distal digital annular ligament promotes stability of the

DIP joint. Forces may be altered by foot conformation; in ahorse with ‘weak heels’ there is greater extension of the DIPjoint than in a horse with ‘strong’ heels, which results inincreased pressure concentrated on the distal aspect of thenavicular bone (Denoix 1999b).

Compressive forces and stress on the navicular bone havepreviously been compared in clinically sound horses andhorses with navicular disease (Wilson et al. 2001). Althoughthe mean peak force and stress were similar, the force andstress in horses with navicular disease were approximatelydouble early in the stance phase of the stride. This early peakstress resulted in a much higher loading rate of the navicularbone in the navicular disease group. The difference in loadingpatterns was associated with an increased force in the DDFT inthe early and mid-stance phases, probably due to increasedcontraction of the DDF muscle. This contraction of the DDFmuscle may result in toe-first ground contact, seen in somehorses with navicular disease. It is suggested that painassociated with the navicular bone may result in positivefeedback, by increasing the force in the DDFT to avoid heel-

Fig 2: Dorsal surface of the deep digital flexor tendon at thelevel of the navicular bone. There is extensive dorsal fibrillation.

Fig 3: Lateral views of 3 feet of varying conformation from 3 horses with navicular disease.

a)

b)

c)


first landing, and hence paradoxically increasing thecompressive force on the navicular bone. This hypothesis issupported by reduction in peak forces on the navicular bonethroughout the stance phase in horses with navicular diseaseafter perineural analgesia of the palmar digital nerves(McGuigan and Wilson 2001).

Although low, collapsed heel conformation hasanecdotally been associated with navicular disease, a recentstudy (Eliashar et al. 2004) in Irish draught-cross-type horsesshowed no correlation between the peak force exerted on thenavicular bone by the DDFT and the conformation of the hoofcapsule, contrary to the earlier results of Denoix (1999b).However, a 1° decrease in angle of the solar border of thedistal phalanx resulted in a 4-fold increase in peak force on thenavicular bone (Eliashar et al. 2004). There was no correlationbetween the angle of the solar border of the distal phalanxand degree of heel collapse.

The shape of the navicular bone may be determined at birthand this may influence the biomechanical forces subsequentlyapplied to the bone, and hence influence the risk ofdevelopment of navicular disease (Dik et al. 2001a,b).Finnhorses and Friesian horses tend to have a straight or convexcontour of the proximal articular border of the navicular boneand rarely develop navicular disease. There is a much higherincidence of navicular disease in the Dutch Warmblood breed,and horses in which the proximal articular margin is concave orundulating appear to be at highest risk of development of thedisease (Dik and van den Broek 1995; Dik et al. 2001a).

Histopathological studies

Navicular disease has not been reproduced experimentally;therefore, all proposed aetiologies remain speculative. Earliertheories suggesting a vascular aetiology with arteriosclerosis(Rijkenhuizen et al. 1989), or thrombosis, resulting inischaemia within the navicular bone (Colles and Hickman1977), have largely been rejected due to failure to identifyischaemic bone or thrombosis, failure to reproduce clinicalsigns or pathological changes by occluding blood supply tothe bone and expanding evidence demonstrating increasedbone modelling (Ostblom et al. 1982; MacGregor 1984; Poolet al. 1989; Wright et al. 1998). Post mortem studies to datehave focused principally on long-term, chronic cases, generallywith advanced radiographic abnormalities, reflecting the endstage of a disease complex. These studies identified strikingsimilarities between the pathological features of naviculardisease and osteoarthritis in both people and horses (Pool etal. 1989; Wright et al. 1998).

Studies of ageing changes in the navicular bone of normalimmature and mature horses suggested that there is adegenerative ageing process similar to that seen in joints(Wright et al. 1998). However, a more recent studyinvestigating not only the navicular bone, but also the DDFT,CSLs, DSIL and navicular bursa demonstrated no age-relateddifferences between mature horses aged 4–15 years with nohistory of foot-related lameness (Blunden et al. 2006a,b). Thissuggests that there may be an individual susceptibility to

degenerative change. Nonphysiological biomechanical factorsmay promote this susceptibility to degenerative change (Poolet al. 1989; Wright and Douglas 1993; Wilson et al. 2001).

The explanation for pain and lameness in horses with nodetectable radiological change has been poorly investigated bypost mortem studies. However, recent clinical experience withMRI has indicated that many horses with evidence of increasedmodelling of the navicular bone, based on increasedradiopharmaceutical uptake (IRU) detected using nuclearscintigraphy, do have pathological abnormalities of thenavicular bone detectable using MRI, with or withoutconcurrent changes in the DDFT, CSLs, DSIL and navicular bursa(Dyson et al. 2005; S. Dyson and R. Murray, unpublished data).

Degenerative changes in the fibrocartilage on the palmaraspect of the navicular bone occur principally in the distal halfof the bone, especially centred around the sagittal ridge in bothsound and lame horses (Blunden et al. 2006a). In horses withnavicular disease there is a greater degree of fibrocartilagedamage, which may extend into the subchondral bone (Figs 1 and 4). Partial thickness loss of fibrocartilage in thislocation was one of the most common lesions significantlyassociated with navicular disease in one study (Wright et al.1998). It is likely to represent some of the earliest pathology ofone form of this disease, but remains difficult to identify in vivo,even with the use of MRI (S. Dyson et al., unpublished data).Degenerative change of the spongiosa is generally seen onlydorsal to extensive fibrocartilage damage. Physiological forcesresult in adaptive remodelling of the subchondral bone inimmature horses, with cortical thickening (Wright et al. 1998).Nonphysiological forces may result in focal fibrocartilage and/orflexor cortex damage, with adjacent subchondral sclerosisdorsal to it, associated with thickening of trabeculae and focalareas of lysis. There may also be oedema, congestion andfibrosis of the marrow stroma within the medullary bone,which may result in a cyst-like lesion.

Concurrently, there may be fibrillation of the dorsal surfaceof the DDFT, which may predispose to adhesion formationbetween the DDFT and regions of partially or fully erodedfibrocartilage on the palmar aspect of the navicular bone.Whether lesions in the DDFT are primary or secondary to pre-existing damage of the fibrocartilage currently remains open todebate. However, recent post mortem evidence suggests thatthere may be nonage-related degenerative vascular and matrixchanges in the dorsal aspect of the DDFT in both lame andclinically normal horses (i.e. similar frequency of occurrence inyoung and old horses) (Blunden et al. 2006b) (Fig 5). Althoughother authors have suggested that vascular occlusion andmatrix changes in the DDFT may be age-related (Wright et al.1998), the results of our study showed that the severity ofthese changes was greater in horses with palmar foot pain thanin control horses. Minor fibrillation of the dorsal aspect of theDDFT was seen in both lame and control horses, whereas deepsagittal splits were seen only in lame horses. Completeocclusion of blood vessels, replacement of normal tendonarchitecture by focal fibroplasia and areas of fibrocartilaginousmetaplasia were common in the lame horses. As these changesare predominantly seen in the intratendonous septa, there is a


strong possibility that they predispose to the development ofsagittal splits in the dorsal surface of the tendon along theseseptal planes. Sharp edges of splits in the DDFT (Fig 6)extending from the dorsal surface may cause ulceration of thefibrocartilage of the navicular bone and thus predispose tolesions extending into the medulla.

There is an association between changes of the flexor aspectand distal and proximal borders of the navicular bone (Blundenet al. 2006a). Similar types of change occur at the proximal anddistal aspects, but tend to be more extensive distally. Enlargedsynovial invaginations are the result of recruitment and activationof osteoclasts following the course of the nutrient vessels intothe spongiosa (Pool et al. 1989). This may be associated withlocal medullary osteonecrosis, and the presence of foci offibrocartilaginous metaplasia and/or entheseous new bone closeto the interface between the DSIL and the navicular bone.

Ageing changes were described in the articular cartilage ofthe navicular bone and the opposing face of the distal phalanx(Bowker 2003). There was loss of proteoglycan and tidemarkadvancement, thought to reflect excessive shear stress in thezone between the calcified and noncalcified articular cartilage.A greater number of tidemarks were seen in horses withclinical signs of navicular disease than normal horses of similarage. However, a more recent study failed to identify significantage-related changes, and low-grade degenerative changes inthe articular cartilage were common in both control horsesand those with navicular disease (Blunden et al. 2006a).

Observations from nuclear scintigraphy and MRI

Previous studies using tetracycline labelling of bone(MacGregor 1984), histomorphometry (Ostblom et al. 1982)and scintigraphy (Keegan et al. 1996) have indicated thatthere is evidence of increased bone turnover in associationwith navicular disease, even in the absence of radiologicalabnormalities of the bone. IRU predominantly reflects

Fig 4: Section from the distal half of the palmar aspect of thenavicular bone. Palmar is to the right. There is complete loss offibrocartilage. There are many reactive chondrones (blackarrows) in the subchondral bone. Bone dust (open arrow) on thepalmar aspect is a processing artefact. H&E; magnification x20.

Fig 5a: Section of a deep digital flexor tendon with partialocclusion of vessels (black arrows) in a pale septum(arrowheads). There is fibrocartilaginous metaplasia within theseptum. Note the chondrones (white arrows). White areasbetween the tendon fascicles are processing artefacts. Hartsvan Gieson; magnification x400.

Fig 5b: Section of a deep digital flexor tendon with earlyfibrocartilaginous metaplasia (black arrows). Several blood vesselsare occluded (arrowhead). White areas between the adjacenttendon fascicles are processing artefacts. H&E; magnification x200.

Fig 6: Section of the dorsal aspect of a deep digital flexortendon with a parasagittal split in the dorsal surface. Dorsal isto the left. Note the mild chondrocyte response and absence ofmarked inflammatory change. H&E; magnification x40.


increased osteoblastic activity (Dyson and Weekes 2003),but is not synonymous with either pain or lameness (Dyson2002). IRU may reflect a functional adaptation to footconformation and the biomechanical forces on the navicularbone. Comparison between scintigraphy and MRI hasdemonstrated that many horses with focal moderate orintense IRU have abnormalities of the navicular bonedetectable using MRI (S. Dyson, unpublished data).However, scintigraphy can also produce false-negativeresults, indicating that pathological abnormalities of thenavicular bone are not always associated with increasedosteoblastic activity.

A comparison of MRI findings in control horses with nohistory of foot-related pain and horses with chronic palmarfoot pain showed significant alterations of the navicularapparatus in the lame horses (Murray et al. 2006a). A

comparative MRI and post mortem study showed goodcorrelation between the lesions identified using MRI andhistopathological findings (Murray et al. 2006b). Clinicalexperience with MRI in horses with foot pain provides supportfor the progression of lesions as outlined above and hasdemonstrated some earlier lesions than those investigatedpost mortem (S. Dyson and R. Murray, unpublished data) (Figs 7–10, illustrating lesions of decreasing severity).

However, a group of horses has also been identified withno detectable abnormalities of the flexor fibrocartilage orcortex, but with diffuse abnormalities of the medullacharacterised by increased signal intensity in fat-suppressedimages (Fig 11). Post mortem examination of one such horserevealed evidence of early fat necrosis with a moth-eaten

Fig 7a: Parasagittal SPGR image of a navicular bone. There is a full-thickness defect in the palmar cortex of the bone (arrow). There is a diffuse area of reduced signal intensitywithin the spongiosa of the bone. On a palmaro45ºproximal-palmarodistal oblique radiographic view there was a focal areaof subtle reduced opacity of the palmar cortex coincident withthe defect in the MR image. No other radiological abnormality was detected. There was focal intense increasedradiopharmaceutical uptake in the navicular bone.

Fig 7b: Transverse SPGR image of the foot in Figure 7a. There isa full-thickness defect of the palmar cortex of the navicularbone medial to the sagittal ridge (white arrow); there isdecreased signal intensity in the medulla in the medial half ofthe bone. There is a sagittal plane split in the deep digital flexortendon (black arrow).

Fig 7c: Parasagittal T2* GRE image of the navicular bone inFigure 7a. There is disruption of the flexor cortex (arrow) andfocal increased signal intensity extending into the subchondralbone. Dorsally there is a diffuse area of intermediate signal inthe medulla. There is endosteal irregularity of the flexor cortexproximally (arrowhead).

Fig 7d: Sagittal STIR image of the navicular bone in Figure 7a.There is focal disruption of the palmar cortex of the navicularbone with a focal area of hyperintense signal extending intothe subchondral bone (arrow). There is a mild, diffuse increasein signal in the medulla.

appearance of the trabeculae (i.e. disruption of the normallysmooth borders of the trabeculae), with necrosis of boneedges. This may have a different aetiopathogenesis.

Hyperintense signal in the medulla of the navicular bonehas been ascribed to the presence of oedema in the marrowspaces (Schneider et al. 2003), but this was not validated postmortem. Further research is required to determine the truecauses of this phenomenon. In our study, mild or moderatefocal or generalised increased signal intensity in fat-suppressedimages was associated with trabecular thinning and widened

intertrabecular spaces (Murray et al. 2006b). High signalintensity in fat-suppressed images associated with irregulardecreased signal intensity in T1- and T2-weighted images wasassociated with generalised osteonecrosis and fibrosis, withirregular trabeculae, adjacent adipose tissue oedema andprominent capillary infilatration. A recent post mortem study offeet with advanced radiological abnormalities of the navicularbone demonstrated that increased signal intensity in fat-suppressed images correlated with areas of degenerate adiposetissues, with haemorrhage or replacement by fibrocollagenousmaterial, or fluid-filled cystic spaces (Busoni et al. 2005).

In some horses, fluid-filled osseous cyst-like lesions havebeen seen in the distal aspect of the bone, apparently separatefrom synovial invaginations, and not associated with anydetectable abnormality of the flexor aspect of the bone (Fig 12). Such lesions have not yet been characterisedhistologically and their aetiology remains speculative,although may be associated with lesions of the DSIL.


Fig 8a: Transverse T2* GRE image of a navicular bone. There isfocal disruption of the palmar cortex of the bone just lateral tothe sagittal ridge (white arrow). There is also mild endostealirregularity laterally (arrowheads). In a palmaro45ºproximal-palmarodistal oblique radiographic view there was anextremely subtle area of reduced opacity within the palmarcortex coincident with this lesion, but it did not appear topenetrate the palmar aspect of the cortex. No other radiologicalabnormality was detected. There was focal moderatelyincreased radiopharmaceutical uptake in the navicular bone.

Fig 8b: Parasagittal T2* GRE image of the navicular bone inFigure 8a. There is a partial thickness defect in the palmarcortex of the navicular bone (white arrow). There is mildendosteal irregularity of the dorsal and palmar cortices of thenavicular bone. Distal to the navicular bone there is loss ofseparation between the distal sesamoidean impar ligamentand the deep digital flexor tendon (black arrow). There is alsoan entheseophyte extending into the collateral sesamoideanligament (open arrow).

Fig 8c: Transverse T2* GRE image of the foot in Figure 8a. Thereis complete loss of separation between the deep digital flexortendon and the distal sesamoidean impar ligament. There is alinear region of increased signal intensity through bothstructures (black arrow). Dorsal to this there is mild endostealirregularity (open arrow).

Fig 8d: Parasagittal STIR image of the navicular bone in Figure 8a. There is a well circumscribed region of hyperintensesignal in the distal half of the bone. There is also increasedsignal intensity in the distal phalanx at the insertion of thedistal sesamoidean impar ligament (arrow).

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Occasionally, horses have been identified with new boneon the palmar aspect of the navicular bone, centred on thesagittal ridge. The cause of this is currently unknown.

Entheseous changes

The presence of entheseous new bone on the proximal borderof the navicular bone, reflecting previous insertionaldesmopathy of the CSL, is well documented radiographically(Verschooten et al. 1989; Wright 1993) and at post mortemexamination (Pool et al. 1989; Wright et al. 1998) in bothclinically normal horses and those with navicular disease. Itsclinical significance remains uncertain, although more extensivenew bone in this location tends to be associated with othersigns of navicular disease (Verschooten et al. 1989; Wright et

al. 1998). Recent experience with MRI has confirmed this(Dyson et al. 2005) (Fig 13). Rarely, an avulsion fracture isidentified at the insertion of the CSL into the navicular bone (S. Dyson et al., unpublished data). Mineralised and osseousfragments in the DSIL have also been recognised in bothnormal horses and those with navicular disease, and theirclinical significance remains difficult to determine. Fragmentswere unusual in sound horses undergoing prepurchaseradiographic examination (Kaser Hotz and Ueltschi 1992),although their true incidence may be underestimated byradiographic examination compared with MRI or computedtomography. In 2 post mortem studies, fragments associatedwith a defect in the distal margin of the navicular bone weremore common in horses with navicular disease than in age-matched controls (Wright et al. 1998; Blunden et al. 2006a).This has also been our clinical experience (Fig 14).

Fibrocartilaginous metaplasia in the body of the DSIL wasmore extensive in horses with navicular disease comparedwith age-matched control horses (Blunden et al. 2006a).However, no significant differences between groups wereseen in the CSLs.

Ageing changes have been seen in the region ofinsertion of the DSIL and the DDFT, with a change infibroblast shape and an increase in proteoglycans (Bowkeret al. 2001). The functional significance of this is not yetknown. Evidence of inflammation has recently beenrecognised histologically at the intersection of the DSIL andDDFT in horses with clinical signs of navicular syndrome (vanWulfen and Bowker 1997). Bowker (2003) demonstratedchanges reflecting ‘abnormal stress’ at the insertion of theDSIL and DDFT in horses with poor foot conformation. Thisregion is rich in sensory nerve endings, with manyarteriovenous complexes which are damaged in horses withnavicular disease (van Wulfen 1999).

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Fig 9a: Parasagittal T2* GRE image of a navicular bone. There isa partial-thickness defect in the palmar cortex of the bone with focal fluid accumulation, reflecting loss of fibrocartilage(black arrow). There is irregular endosteal mineralisation (openarrow). There was no significant radiological abnormality andradiopharmaceutical uptake was normal.

Fig 9b: Transverse T2* GRE image of the navicular bone in Figure 9a. There is focal fluid accumulation palmar to the bone(arrow) reflecting fibrocartilage loss. Abaxial to this the deepdigital flexor tendon is in close apposition to the bone andprobably adherent. Dorsal to the fluid accumulation there isfocal endosteal mineralisation (open arrow).

Fig 9c: Parasagittal STIR image of the navicular bone in Figure9a. There is focal fluid accumulation palmar to the navicularbone (white arrow) reflecting loss of fibrocartilage. There islinear increase in signal intensity through the middle of thebone (arrowheads) and extending into the distal sesamoideanimpar ligament.

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result of abnormal stresses at the attachments of the CSL andDSIL on the navicular bone, and this may reflect a differentmechanism of navicular disease development.

Although endosteal irregularity at the insertion of the DSILon the distal phalanx may be seen in both horses with andwithout foot pain (Murray et al. 2006a,b), in some lame horsesthere is evidence of insertional desmopathy, characterised byaxial cortical disruption and/or increased signal intensity in thebone at this site in fat-suppressed images, reflecting boneoedema or necrosis (S. Dyson and R. Murray, unpublished data).

The navicular bursa

The incidence and aetiology of primary bursitis of the navicularbursa is not known, nor is its relationship to the developmentof navicular disease. Villous hypertrophy, hyperplasia ofsynovial lining cells and venous congestion have beendescribed in association with navicular disease, whereas thesynovial membrane appeared uniform in 6 normal horses ofundetermined age (Svalastoga and Nielsen 1983). However, inanother study comparing immature horses, those withnavicular disease and age-matched controls, 3 of 25 age-matched controls had evidence of asymptomatic chronicsynovitis. In both the navicular disease group and the age-matched controls, mild hyperplasia and hypertrophy was seencompared with immature horses up to 3 years of age (Wrightet al. 1998). In a more recent study, there was no evidence ofacute inflammation within the navicular bursa in horses withpalmar foot pain or age-matched control horses (Blunden et al.2006a); however, lame horses had marked chronic synovialproliferation compared with control horses (Blunden et al.2006a; Murray et al. 2006a). There was a positive associationbetween abnormalities of the bursa and lesions of either thedorsal aspect of the DDFT or the flexor aspect of the navicularbone. Clinical experience with MRI has indicated that abnormaldistension of the bursa is a frequent finding in lame horses, butis rarely seen in isolation (Dyson et al. 2005) (Fig 16).

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Fig 10a: Parasagittal SPGR image of a navicular bone. There isendosteal irregularity of the dorsal and palmar cortices (whitearrows) and a mineralised line in the palmar distal aspect of thebone, distal to which is an area of intermediate signal intensity(black arrow). There is entheseophyte formation proximally (openarrow). There were 2 small, well-circumscribed radiolucent areasproximal to the distal border of the navicular bone. There was mildfocal increased radiopharmaceutical uptake in the navicular bone.

Fig 10b: Transverse SPGR image of the navicular bone in Figure 10a. There is a parasagittal split in the deep digital flexortendon (black arrow). There is endosteal irregularity of theopposing palmar cortex of the navicular bone (white arrow).Note also the diffuse hypointense signal in the palmarprocesses of the distal phalanx (open arrows).

Fig 10c: Parasagittal STIR image of the navicular bone in Figure 10a.The same mineralised line is seen in the palmar distal aspect of thebone, distal to which is an area of increased signal intensity.

Clinical experience with MRI has demonstrated thatstructural abnormalities of the DSIL are often seen in associationwith abnormal modelling of the distal palmar aspect of thenavicular bone, with focal increased signal intensity in fat-suppressed images (Dyson et al. 2005) (Figs 8c,d and 13). Oneauthor has suggested that this focally increased signal intensityin the distal aspect of the navicular bone at the origin of theDSIL on fat-suppressed images may represent an important earlyevent in the aetiopathogenesis of navicular disease (Schneideret al. 2003). Increased signal intensity may also be seen in thenavicular bone close to the insertion of the CSLs in fat-suppressed images (Dyson et al. 2005). In some horses there isa linear band of hyperintense signal in fat-suppressed images,extending through the middle one-third of the navicular bone,from the insertion of the CSL to the origin of the DSIL (Fig 9c).Abnormalities of the CSL have also been associated withconcurrent abnormalities of the navicular bone (Fig 15). Basedon our clinical experience, it seems that these lesions may be the


Associations between injuries

It is clear from our recent post mortem study, and fromclinical experience using MRI, that frequently severalstructures are affected concurrently. It is common to seevarious combinations of abnormalities of the navicularbone, DDFT, DSIL, CSL and collateral ligaments (CL) of theDIP joint. Clinical MR examination of 263 horses withforelimb foot pain revealed 6 with abnormalities of thenavicular bone alone; 29 with concurrent DDFT andnavicular bone abnormalities; 60 with various combinationsof abnormalities of the navicular bone, DSIL, DDFT or CSL;46 with CL injury of the DIP joint in combination withlesions of the DDFT, CSL, DSIL or navicular bone; and 25 horses with abnormalities of 5 or more structures (S. Dyson and R. Murray, unpublished data). The sequence

of injury occurrence remains speculative. It is possible thatdegenerative changes in several structures may predisposeto concurrent injury. The navicular bone, CSL and DSIL actas a unit, so presumably undergo similar biomechanicalstresses. Alternatively, injury to one structure may cause low-grade instability, predisposing to injury of closely related structures.

What causes pain?

Pain associated with navicular disease may be due to venouscongestion of the navicular bone. Dilated venules andsinusoids entrapped in fibrous marrow have only beenidentified in horses with navicular disease (Pool et al. 1989).Raised intraosseous pressure has been measured in horseswith navicular disease (Svalastoga and Smith 1983; Pleasantet al. 1993). Distension of the navicular bursa may causepain. The contribution of other causes or sources of painremains open to speculation, although many sensory nerveendings have also been identified in the CSLs and DSIL(Bowker et al. 1993, 1997) and, given the high frequency of occurrence of concurrent abnormalities in thesestructures, it is likely that these nerve endings may beimportant in pain mediation.

Fig 11c: Histological section of the navicular bone in Figure 11a.There is marked disruption and necrosis of the adipose tissue. The trabeculae have a moth-eaten appearance (arrows).H&E; magnification x200.

Fig 11a: Sagittal SPGR image of a navicular bone. There isdiffuse hypointense signal throughout most of the navicularbone. No significant radiological abnormality was detected;radiopharmaceutical uptake in the bone was marginally increased.

Fig 11b: Parasagittal STIR image of the navicular bone in Figure 11a. There is diffuse hyperintense signal throughout themajority of the bone.

Fig 11d: Transverse SPGR image of the same foot as Figure 11a,just proximal to the navicular bone. There is a parasagittal splitof the lateral lobe of the deep digital flexor tendon (arrows).


Fig 12a: Parasagittal SPGR image of a navicular bone. There is amineralised band traversing from the dorsal to palmar cortices(arrows), distal to which is a diffuse area of intermediate signalintensity. There was a single axial discrete radiolucent zoneproximal to the distal border of the bone and mild focalincreased radiopharmaceutical uptake in the bone.

Fig 12b: Parasagittal T2* GRE image of the navicular bone in Figure 12a. There is a similar mineralised band traversing from thedorsal to palmar cortices of the bone (arrows), distal to which is anarea of hypointense signal, consistent with proteinaceous fluid.

Fig 12c: Parasagittal STIR image of the navicular bone in Figure 12a. There is a band of mineralisation from the dorsal topalmar cortices (arrows), distal to which is a diffuse area ofhyperintense signal.

Fig 13a: Sagittal T2* GRE image of a navicular bone. There is anentheseophyte (arrow) in the collateral sesamoidean ligament.There is slight endosteal irregularity of the dorsal and distalcortices. There was slight irregularity of the proximal and distalborders of the bone seen radiographically. Uptake ofradiopharmaceutical was normal.

Fig 13b: Dorsal SPGR image of the navicular bone in Figure 13a. There is marked irregularity of the proximal anddistal cortices axially. Note also the focal area of intermediatesignal proximal to the distal border of the bone axially (arrow).

Fig 13c: Sagittal STIR image of the navicular bone in Figure 13a. There is focal hyperintense signal immediately distaland dorsal to the insertion of the collateral sesamoidean ligament(black arrow). There is focal hyperintense signal proximal to andextending into the distal sesamoidean impar ligament (whitearrow). There is a focal area of fluid accumulation palmar to thebone midway between the proximal and distal borders of thebone (open arrow), reflecting loss of fibrocartilage.


The future

It is clear that degrees of adaptive and reactive change occurin the navicular apparatus of all horses. We need tounderstand better both the factors that stimulate theirprogression and what causes pain. Identification of geneticand biomechanical risk factors would be useful. Study of earlycases of navicular disease should help to establish better theinterrelationship between abnormalities of the DDFT, navicularbone, CSL and DSIL. We need to determine what factors leadto vascular and matrix changes in the DDFT. Further researchinto the sensory nerve supply to the navicular apparatus mayhelp in understanding what causes pain and thereforelameness, and how it may be treated.

Acknowledgements

We thank The Home of Rest for Horses for financial support.

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Documents

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