Part I: Operative Orthopedics of the Fetlock Joint of the ... · Part I: Operative Orthopedics of...

Part I: Operative Orthopedics of the FetlockJoint of the Horse: Traumatic andDevelopmental Diseases of the EquineFetlock Joint

Larry R. Bramlage, DVM, MS

The invitation to present the Frank J. Milne State-of-the-Art Lecture is a special degree of flattery forone’s career. The flattery comes with a degree of responsibility to present the current state ofpractice and, to a certain extent, challenge doctrine and lay out theories of practice that result fromone’s years of practice in a specialty area. The lecture should, therefore, enjoy the possibility ofmoving the “state of the art” forward. In areas where the author of this manuscript has a view ofpathology that varies from the current concepts, the views will be presented as theories based onyears of observation and, where possible, controlled studies. The object is to lay them out forexamination and challenge or refutation by future practitioners of this specialty. I want to thank themembers of the American Association of Equine Practitioners for this opportunity. Author’s ad-dress: Rood and Riddle Equine Hospital, PO Box 12070, Lexington, Kentucky 40580; e-mail:[email protected]. © 2009 AAEP.

“An orthopedic surgeon must be able to thinklike a bone, and feel like a joint.”—Anonymous

1. Introduction

The fetlock joint is, arguably, the joint that makes ahorse a horse. Its unique anatomy and physiologyallow the high-speed, medium-distance activity thathas lead to the unique place for the horse in society,historically and currently. Its evolution allowedthe horse to become a single-digit quadraped. Thefetlock is a joint, a shock absorber, an energy storagesystem, and a stabilizer of the distal limb.1,2 It is

constructed like a suspension bridge with structuralmembers incapable of supporting its loads until theappropriate ligament tenses and supports the bone.It is the most fascinating of the complex of jointsthat allows a horse to move at high speeds and overrough terrain with little conscious concern. Be-cause of its complexity, it is vulnerable to a varietyof traumatic and developmental problems that arethe veterinarian’s purview.

This paper will discuss the traumatic and devel-opmental diseases of the fetlock joint and concen-trate on the physical causes and surgical treatmentUnreferenced statements are the opinion of the author.

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NOTES

of diseases of the fetlock joint. Space and time lim-itations will preclude details of surgical techniquefor most procedures. Concepts will be presentedand surgical techniques will be referenced wherepossible.

2. Defining the Problem

Short of a fracture needing the reconstruction of anarticular surface, the majority of clinical problems inthe fetlock joint present a risk for secondary degen-erative arthritis as their sequelae. To reach thepoint of a decision to treat the fetlock joint surgi-cally, we must be able to understand the concept ofprogressive degeneration, to assess the current sta-tus of the joint, and to understand when the surgeoncan make a difference.

Primary degenerative arthritis is rare in thehorse.3 What we see in the horse is degenerativearthritis secondary to an insult of traumatic or de-velopmental origin. The overwhelming volume ofliterature in recent years has concentrated on thebiology of the degenerative arthritis cycle. This pa-per will concentrate on debris in the joint, the re-sultant physical damage, and the biologic responsesthat it initiates.3,4

The physical debris liberated into the joint as partof the original insult and by the joint’s attempt toheal mediates most of the ongoing damage after atraumatic or developmental osteochondral frag-ment. If the cause is developmental or traumatic,the secondary reaction of the joint is remarkablysimilar.5 So, it follows that the treatment will besimilar as well. When one examines the reaction ofthe joint to a traumatic disease such as an osteo-chondral fragment or to a developmental abnormal-ity such as an osteochondritis dessicans (OCD), theplace where the two inciting causes are similar is inthe shedding of debris into the joint.

Debris is physical (particulate) and biologic (in-flammatory cytokines/mediators of inflammationthat are liberated by the chondrocytes and synovio-cytes, and inflammatory cells recruited to the jointby response to the physical insult). As the debris isliberated the joint responds to the insult. Injectionof cartilage particles experimentally can create sy-novitis and mechanical injury to cartilage, but bonedebris is likely more important and more damag-ing.6,7 Removal of the inciting lesion and its asso-ciated debris allows the joint to return normal if thesecondary arthritis has not reached the criticalthreshold of self-perpetuating degeneration.

Degenerative joint disease (DJD) has sometimeserroneously become a “catch all” for any change seenon radiographs. Most joint inflammation seen inthe equine athlete is not degenerative, especially inyoung horses; it is the response to traumatic ordevelopmental insult. The response to trauma or adevelopmental OCD lesion is often reversible earlyin the course by removing the inciting cause, andtherefore, it is not degenerative.

Degenerative arthritis certainly will occur if theinciting cause is left unattended and the destructionprogresses to the point that it will proceed unabatedeven if the cause is removed. But, fortunately,lameness and decreased performance usually occurin horses in strenuous activities before the jointreaches this state, providing the opportunity for di-agnosis and treatment of the primary disease beforeit becomes irreversible.

The clinical signs can be subtle, especially if thelevel of the horse’s activity is moderate. In theauthor’s experience, the attending veterinarian forhigh-level equine athletes has an advantage in thathorses in heavy work will show more significantsigns than horses in light activity, although thejoint’s response is the same in total. High-levelactivity elevates the rate of debris shedding andmagnifies the joint response, but hypothetically, theamount of debris shedding seems to be a direct prod-uct of the severity of the problem and the activitylevel of the horse. Horses with small problems orlow levels of activity may shed debris at a rate thatcauses a subtle joint response, creating lamenessthat remains subclinical. But low-level clinicalsigns are indications for concern and eventually, cancause acute significant lameness, because, in theauthor’s opinion, when debris shedding approachesa critical mass, the clinical damage will be similar.

The need for treatment is obvious with acute dam-age such as a dorso-medial proximal phalanx (P-I)chip fracture of the fetlock joint in a racehorse, be-cause the debris shedding is acute, the damage tothe joint is rapid, and it causes lameness early in thecourse of the disease. But, a show horse or a plea-sure horse with a similar lesion may show only mildsigns, such as effusion and pain on flexion, but nolameness. Although the debris shedding may beslower in less strenuous activity, clinical observa-tion suggests slower shedding causes lameness andcauses joint damage after a comparable amount ofdebris is shed.

The need for treatment in the racehorse is obviouswhen it cannot perform because of lameness. Theneed for treatment for a similar injury in the horseof less strenuous activity may be less clear whendebris shedding causes only the synovial effusion,but the horse can still perform. The permanentdamage accumulating in the joint is less obvious,because the rate of damage is slow but the end effectis no less severe. After the same amount of debrisis liberated, although it takes a much longer time,the end result is equally severe.8

The determination of the need for treatment inthe pleasure or working horse with subclinical dis-ease is more difficult. Not all horses’ careers arevaluable enough to warrant surgical intervention forall conditions. Simply the fact that the horse canperform is not an indication that the fragment isinnocuous, especially if the horse requires ongoingintra-articular therapy to mitigate the signs. Oftena fragment will be tolerable for a prolonged period of

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time, especially with intra-articular medication.If the horse is easily replaceable or its use can beeasily changed, then the decision may be to toleratethe problem. But, if it is unacceptable to risk hav-ing the horse’s disease progress and potentiallyshorten the athletic career, then fragment removalis the best treatment. So, each diagnosis of poten-tial damaging traumatic fragmentation or develop-mental bone malformation must be evaluated inlight of the long-term effect on the horse’s career andperformance level. The decision to remove or totolerate the presence of a fragment needs to be anactive one and not simply a matter of assuming thatminimal clinical lameness means no harm.

Economic realities must figure into the evalua-tion. Early surgical removal requires an upfrontexpense but with the good prospect of permanentlysolving the disease.9–11 Forgoing the surgicaltreatment of the fragment and treating it medically,especially with symptom-modifying medications,will be progressively expensive over time and willameliorate the signs but not stop the progression ofthe disease. Eventually, the debris shedding candamage the hyaline cartilage to the degree that itwill disable the joint. This can end or denigrate thehorse’s career after a few years, necessitating re-placement of the horse before the end of the horse’snatural career span. Medication may be able torelieve the clinical signs or interrupt the biologicprocesses of joint inflammation by negating the bio-logic debris, (inflammatory cytokines/mediators ofinflammation that are liberated by the chondrocytesand inflammatory cells recruited to the joint by re-sponse to the physical insult) but it will not stop thephysical debris shedding, which continually takesits toll on the hyaline cartilage. Owners and someveterinarians mistakenly assume that the mitiga-tion of clinical signs is a cure, especially in high-class performance horses that can afford frequentintra-articular therapy. They assume that fre-quent joint injections are “simple maintenance.”Then, when the “maintenance” no longer “main-tains” the joint, they are confused about the lack ofresponse and consider surgery as a treatment.The worst choice that can be made is to medicallytreat a horse with a surgically resolvable disease,allow the joint to suffer irreversible damage, andthen attempt to surgically remove the cause. Thisprovides the worst of both possibilities: the mostpossible expense and the shortest possible career.

The irreversible change in a joint is the loss of thestructural aspect of the hyaline cartilage, primarilythe collagen. The chondrocyte population is labilebut has some reproductive capability if the insult isnot overwhelming.3,12 The physiologic componentof the cartilage maintained by the chondrocytes, theproteoglycan, is replaceable; in fact, it is in a con-stant state of flux, normally in equilibrium, withproduction equaling destruction.3 In inflammatoryconditions, the production may be slowed or thedestruction may be accelerated, tilting the balance

to a deficit in proteoglycan balance, but simple pro-teoglycan depletion is reversible.

The lubricating function of the proteoglycan pro-tects the collagen in the normal joint. In the dis-eased joint, the proteoglycan becomes depleted, andthe collagen becomes exposed and vulnerable. So,any measure that preserves proteoglycan function,its lubrication of the cartilage surface, and there-fore, its protection of the collagen is likely worth-while to consider for the prevention of collagendegeneration and degenerative joint disease/degen-erative arthritis. This is where the disease-modi-fying medications have an important potential forbenefit and again caution should be exercisedwith use of medication that is only symptom-modi-fying.13 This is also where surgery can shine if thecause is removable and the rest of the joint is stillnormal.

Extensive or prolonged loss of proteoglycan com-bined with use of the joint makes the cartilage col-lagen architecture so vulnerable to wear that itallows permanent damage in short order in the formof destruction of the collagen “backbone” of carti-lage.3,14 Some medical treatment is aimed princi-pally modifying the proteoglycan balance in thejoint.13 No treatment, medical or surgical, has yetshown the ability to produce quality collagen re-placement of the type of collagen architecture that ispresent in hyaline cartilage.5,12,14

The subchondral bone architecture is very impor-tant in its support of the collagen in the correctconfiguration for joint function.15,16 The bone de-termines the anatomy and keeps the cartilage in thecorrect location to articulate with its opposing jointsurface. The calcified cartilage on the surface ofthe bone also serves as the anchoring point for thecollagen of the cartilage. Bone can be replaced, butit is very difficult, nearly impossible, to replace thecalcified cartilage/subchondral bone contour and itsperfectly adapted anatomy of the normal joint.17

Therefore, the collagen’s role in normal joint func-tion requires the anatomy of the bone to bepreserved.

Collagen can be created and proteoglycan can bereplaced, but the body is unable to recreate thearching configuration of the collagen architecturethat anchors hyaline cartilage to the bone.15,17,18

It is this architecture that is required to reach thefunctionality of hyaline cartilage, and it is this ar-chitecture that is missing from fibro-cartilage that isformed after hyaline cartilage loss. “Hyaline-like”replacement fibro-cartilage has proteoglycan con-tent and collagen but not the collagen architecturethat it takes to stand up to exercise in the horse.Therefore, it is at this point impossible to recreatenormalcy in a damaged joint surface in an adulthorse by any means. The lack of a solution fordegeneration places a premium on prevention.

In degenerative arthritis, the collagen is wornfrom the joint surface into the middle and deeplayers of cartilage because of failure of the lubrica-


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tion/protection mechanism and the physical effectsof the debris. The superficial layer of the cartilagecontaining the tops of the arches of collagen is lostfirst (Fig. 1). This exposes the collagen, initiatingthe process we recognize as fibrillation of the carti-lage. With fibrillation, the low-friction joint sur-face is converted into a higher friction joint surface,lubrication becomes more difficult, proteoglycan lossaccelerates, and physical wear overwhelms the car-tilage’s resistance to wear, resulting in progressiveloss of joint function. This process can be acceler-ated or mitigated with exogenous joint therapy, sys-temic or local. Texts and manuscripts arevoluminous on this subject in the literature.19

Hyaline cartilage is resistant to repair, because ithas no blood supply, and it must be replaced byfibro-cartilage; however, fibro-cartilage does nothave the collagen arches that provide the resistanceto joint loading and wear unique to hyaline carti-lage. Fibro-cartilage has an irregular haphazardcollagen arrangement with cross linking of the fibro-cartilage. Further, the anchorage to the bone is be-lieved to be different than native cartilage. Fibro-cartilage can be compared to covering a joint surfacedefect with a scar, which it does effectively, but maynot participate in joint function to a similar extentas native cartilage. Clinically in the horse and insome experimental studies, fibro-cartilage functionswell to cover a defect in the joint surface that pene-trates the subchondral bone, but does not resistwear effectively and under heavy loading, especiallyin shear, fails and detaches from the bone itcovers.17,18,20

Bone can heal but has difficulty restoring joint-surface architecture. Unless bone healing restoresthe innate joint anatomy perfectly, the repaired jointsurface is suboptimal for weight bearing, becausethe fibro-cartilage covering the injured bone does notreach perfect articulation with the opposing jointsurface.

Taken together, the repair process for bone andcartilage of an injured joint surface is poor andachieves success as a scar but not as a functionalreplacement.21 This can result in prevention of in-flammation in some cases, but the scar cartilage andderanged bone anatomy is not completely thought torestore normal joint function to the injured joint.

3. What Is Surgically Possible?

Surgical reconstruction of a joint surface wheneverinstability is present and preservation of as mucharticular surface as possible is a prime indication forsurgical treatment. But, when a joint is injured,most treatments consist of removing the damagedarea to negate the ongoing effects of the injury.The joint resumes function using the preserved nor-mal hyaline cartilage and to some extent the re-paired surface. One cannot rely on a significantarea of repaired joint surface to function for highlevel athletic activity.

The most theoretically promising approaches aresurgical techniques such as microfracture resurfac-ing, and cartilage augmentation and implantationsystems.22–24 Unfortunately they have yet toachieve routine clinical success in the horse.23,24

Any injury over 1 cm in diameter, even in a person,has difficulty resisting the loading asked of a re-paired joint surface, even with the added benefit ofmicrofracturing (Fig. 2).25–27 In the author’s opin-ion, microfracturing injured joint surfaces on thedorsal condyles of the cannon bone or on the articu-

Fig. 1. This diagrammatic representation of articular cartilageillustrates the collagen structure of hyaline articular cartilage.(Modified from Blue Histology of Skeletal Tissues, School of Hu-man Biology, University of Western Australia).

Fig. 2. This intra-operative photograph shows a distal McIIIarticular surface ulcer that has been treated with multiple micropick sites used to fracture the denuded subchondral bone.


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lar surface of the sesamoid bones has not aided inrecovery from the damage to those areas that badlyneed a treatment solution. These are such heavilyloaded articular surfaces that asking fibro-cartilageto perform functionally is not likely feasible.6

Injuries that violate the subchondral bone platecan recreate a superior fibro-cartilage, because thefibro-cartilage can anchor on the exposed cancellousbone effectively.15 However, a deficit in the bonerarely fills to the degree that the bone becomes con-gruent for weight bearing; so, the cartilage is an-chored well and does not fail, because it is in aprotected environment below the normal articularsurface and overlying cancellous bone. But, it doesnot participate in the function of the joint; therefore,it is of a high quality histologically but is of little usefunctionally to the horse.

Injuries that remain weight bearing, even if mi-crofractured, seldom maintain the fibro-cartilage inthe face of serious weight-bearing exercise, becausethe collagen anchorage is insufficient to resist theforces of weight application and is quickly shearedfrom the subchondral bone. Removing the sub-chondral bone plate totally to expose cancellous bonehelps the collagen anchor to the bone; however, itdoes not achieve function, because the normal archi-tecture is destroyed to the point that joint functioncannot be preserved. Forage of damaged subchon-dral bone with multiple drill holes improves anchor-age, but does not produce enough functionalcartilage to restore joint function. It is most likelyimpractical over a large area in the horse, becauseprolonged protection from loading while a functionalfibro-cartilage forms is not possible.17,18

In the author’s opinion, grafting of cartilage, chon-drocytes, or stem cells faces the same difficulty inestablishing an attachment to the subchondral boneas does granulation tissue trying to form fibro-car-tilage. Mosaic-plasty (taking small plugs of carti-lage and bone from a remote site and inserting themin a denuded area) has been tried, but lack of equiv-alent donor sites, stabilization of the plugs, and re-construction of a functional anatomy withoutdamage to the transplanted grafts have all limiteduse.28,29 Prosthetic replacements in horses, as inpeople, have little chance to survive the biomechan-ics of the much larger horse and recreate an athletein the horse or in fact, in people.

Biologic therapy such as stem cells and platelet-rich plasma is being used and shows promise inaiding joint function, but it is currently not able tosubstantially replace articular cartilage during me-chanical loading with the loads that are seen in thehorse.30

So, surgical replacement or augmentation of aninjured joint surface is to this point not a reality.If injured joint surfaces can be reconstructed usinginternal fixation to reconstitute the original anat-omy with the original cartilage surface intact ornearly so, surgery shines.

4. The Role of Surgery

The primary role of surgery is to stop debris shed-ding and restore stability. This is not to disparagethe role that surgery plays in the approach to arthri-tis. It emphasizes the role of prevention of arthri-tis, which is surgery’s strength, rather than thetreatment of arthritis, which is its weakness. Witha few exceptions, surgery is primarily a bone treat-ment in the horse. Surgery stabilizes the recon-structable joint surfaces and removes the damagedbone that would shed debris and further injure thejoint. The joint must survive on whatever cartilagecan be preserved by reconstruction or by preventionof the degeneration mediated by debris sheddingand the subsequent cascade of inflammation thatleads to degeneration (Fig. 3).

5. The Role of Medication in a Joint

Symptom-modifying medications can decrease or re-solve the clinical signs that accompany arthritis andcan be quite useful at buying time for the joint toheal itself, but they can be abused if they are used tocover up a physical problem that continues to dam-age the joint.4,30 They should be used with a thor-ough understanding of their benefits as well asdisadvantages to the joint. When used to simplycover up a physical injury that results from shed-ding debris, obtunding the inflammatory responsewill eventually allow the physical injury to disablethe joint (Fig. 4). Disease-modifying medicationscan promote proteoglycan anabolism, prevent de-struction, and to some extent, negate biologic debristhat damages the joint, but they cannot stop physi-cal debris shedding within the joint that resultsfrom unstable bone.13 It is the physical debris that

Fig. 3. Intra-operative picture of a dorsal P-I chip fracture re-moval shows the effect of debris shedding on the articular surfaceof the distal metacarpus (on the right of the picture). Note thescore lines and cartilage fibrillation. The fragment has beenremoved from the left side, exposing healthy subchondral bone(P-I).


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is shed from traumatic and developmental lesionsthat does the ongoing permanent damage to thehyaline cartilage and therefore, to the joint.5

To understand the reason for the ongoing damagea traumatic fragment of bone or developmental frag-ment of cartilage and bone causes on normal jointsurfaces, one must review the way bone heals in theunstable situation and understand the concept ofcontinual debris shedding. To conceptualize theunstable fragment of bone as a “stone in your shoe”far underestimates the pathology done by an unsta-ble fragment.

6. Gap-Strain Bone Healing and Its Effect on the Joint

Bone has the capability to exactly reconstruct itselfafter fracture injury. It can do this through twoprimary mechanisms. If it is stable, bone can fill agap with new bone (primary bone healing) and re-model to re-establish pre-injury anatomy. This willnormally occur only in the case of a fracture that isnon-displaced or has been surgically stabilized.In unstable bone healing, the bone goes through aseries of steps to attempt to fill the gap between thebone ends with other tissue, which eventually con-verts to bone (secondary bone healing).31–34

The relative motion of the bones in relation toeach other dictates the kind of tissue that formsbetween the fracture ends in secondary bone heal-ing. This “strain” between the bone ends is definedby the “change in length of the gap (motion) dividedby the unit length (the gap).”30–33 In a fracture, theamount of strain at the fracture gap can be restatedas “the amount of motion divided by the size of thegap.”31–34

Bone is a very stiff and strong structure and assuch, has a very low strain tolerance until rupture,�4% in cortical bone and �5% in membranous bone.In stable situations, motion is not a factor, because

the motion and therefore, the strain is under 4% andthe gap can easily fill with replacement bone.31–34

In unstable situations, the strain is greater than thebone can tolerate and therefore, newly formed bonesimply ruptures. Cartilage has a 15% strain toler-ance, so it can tolerate 3–4 times more motion thanbone; granulation tissue or immature fibrous tissuehas a 100% strain tolerance.32,33 Therefore, withhigh motion between the two ends of a fracturedbone, the bone must start by forming granulationtissue, because it will tolerate the highest strain.As more granulation tissue forms and the tissueholding the two ends of the bone together enlarges,it becomes stiffer, thereby reducing the strain be-tween the bone ends. The reduced strain allowsless strain-tolerant tissue such as cartilage to thenform, and the mass, known as callus, gradually cre-ates a union by progressively enlarging and stiffen-ing until it becomes stiff enough to form bone.34

We recognize this process in most fracture healingby the expanding callus that eventually stabilizesand unites a fractured bone, which then reorganizesand replaces the callus with the stronger, smaller,and more organized bone.

Because this process of secondary bone healing bycallus is controlled biomechanically and dependenton the local biomechanics of the gap-strain healingprocess, which is a ratio, the gap size and motion areboth important. The surgeon can facilitate healingby reducing the strain by fracture reduction, immo-bilization, and restriction of exercise, and by align-ing the bone ends to a normal anatomicalconfiguration, because the ends of the bone must bein close proximity to allow favorable local biome-chanical conditions to unite the bone. Counterin-tuitively, a very small gap will have a higher strainthan will a large gap (motion divided by a smallnumber results in a higher strain than the samemotion divided by a larger number). To reducestrain, the gap must enlarge before healing can oc-cur. We recognize this process when unstable frac-tures get wider radiographically, increasing the gap,before they begin to heal (Fig. 5).

If the strain is �100%, it is too high to allowgranulation tissue to unite the bone, and the gran-ulation tissue simply covers the raw bone ends as itdoes in any raw bone surface in a joint. Increasingthe size of the gap, as long as the bone ends are stillapproximated and aligned and the strain can bereduced below 100%, will aid fracture healing.Increasing the gap will reduce the strain, help to getit below the 100% limit of granulation tissue, andallow the callus process to begin, because fracturegap strain is a ratio (motion divided by the gap size).This is a locally mediated phenomenon stimulatedby the local conditions surrounding the fracture.The radiographic widening results from softening ofthe bone by demineralization and disorganization ofthe bone, opening the space between the pieces ofthe fractured bone, reducing the strain, and allow-ing secondary bone healing to proceed. This is a

Fig. 4. This intra-operative photograph shows complete ulcer-ation of the articular cartilage from the dorsal aspect of the distalMcIII as a result of a chronic OCD fragment of the distal abaxialjoint margin.


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novel and effective way to promote fracture healingif the bone is not loaded at the time.

This same process occurs in the joint when a frag-ment is present. Healing between the parent boneand fragment is attempted, but this is a very high-strain environment because the motion is high in ajoint and the gap is very small. Therefore, the par-ent bone actively softens and disorganizes to try toopen the gap and allow healing to occur. But, if thebone is loaded during this process, it breaks up andis shed as it is demineralizing. Marked reductionof motion will sometimes accomplish healing, and achip fracture will heal. Even cast immobilization isnot enough to heal most fragments, and the second-ary bone healing process persists and accelerateswith resumption of exercise. Because of the load-ing with motion, this progressive destruction of theparent bone at the interface with the fragment orOCD results in tremendous amounts of bone matrixand mineral continually shedding into the joint.This constant debris shedding is the primary causeof the degeneration of a joint rather than the pres-ence of the fragment and the “stone in your shoe”

phenomenon. In most joints, fragment stability isnot possible to achieve.

Continued attempts at healing unstable frag-ments occur if raw bone is exposed with resultantdebris shedding progressively damaging the joint.In instances of strain in excess of what the bonehealing process can tolerate, neutralization of rawbone interfaces will eventually occur by covering thebone surfaces with granulation tissue, and if it can-not reduce the strain to �100%, then it matures intofibro-cartilage by the cartilage healing process; thisis the same scar cartilage that covers all raw bonesurfaces in the joint. But, after fibro-cartilageforms, high-level use can erode this cartilage as itdoes in all high-load situations, exposing bone again,stimulating secondary bone healing, and reignitingthe debris shedding. Clinically, the degree of suc-cess of fragment neutralization by fibro-cartilageparallels the degree of success of joint surface heal-ing by fibro-cartilage. In the author’s experience,fibro-cartilage can be functional for less strenuoususes, but for increasing athletic activity, the proba-bility of erosion of the fibro-cartilage and reinitiationof debris shedding increases with the level of ath-letic activity.

If the fibro-cartilage fails when exercise resumes,the parent bone again responds by trying to increasethe gap size to reduce the strain and heal the bone.The fragment can also respond in the same way if itretains sufficient blood supply, but this is not usu-ally the case. The reaction can be identified radio-graphically as demineralization at the interface of amobile fragment and can be seen with the arthro-scope as the softening of the parent bone, which ismaking an attempt to heal the fragment. The moststriking evidence, however, is on the normal carti-lage surface where the debris gets interposed be-tween the cartilage surfaces and physically scoresthe normal cartilage. These “score lines” destroythe superficial layer of articular cartilage where thepinnacles of the arcades of collagen normally formthe tough, gliding surface of the articular cartilage.This damage is permanent and tolerated to a point,after which enough loss of the superficial layer ofcartilage has occurred that the cartilage can nolonger protect itself and it erodes to bone.

The fact that chip fractures are not created by asingle event and are the result of repetitive traumaamplifies this response. So, by the time the frag-ment separates radiographically, the bone deminer-alization and softening is well underway fromattempted healing, and debris has already beenshed into the joint. Since this is an inflammatoryprocess it is hyper-vascular, though the fragmentitself is often avascular.5 This process is an activeresponse, which is minimally influenced by the sizeof the fragment. Even small fragments stimulatethe softening by the parent bone over a large area,shedding debris and doing permanent damage to thejoint. The size of the parent bone/fragment inter-face influences the amount of debris shed at one

Fig. 5. This radiograph shows a medial condylar fracture thatwas not stabilized surgically and has widened the fracture gap toreduce the strain. This is part of the healing process for anunstable fracture.


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time and the rate of damage to the normal joint.Mobile fragments stimulate the debris shedding intothe joint, and the response to traumatic and devel-opmental fragments becomes indistinguishable andends with the same result.5

Many interpret the cause of pain and lamenessfrom a chip fracture as direct physical injury to thejoint surface. This is rarely the case. Cartilagehas no nerve endings with which to generate pain.The pain originates in the subchondral bone due tothe inflammation associated with attempts to healthe chip fracture, and from the interior of the jointas a consequence of the inflammation and distur-bance in joint lubrication mechanisms caused by theinflammation.35,36 The healing process results intrauma from small particles of bone being shed aswell as creating biologic debris, such as interleu-kin-1 �, which promotes the synovial inflammationand cartilage destruction that are the subject ofmuch joint research and the target of all jointtherapy.19

The primary traumatic injury with secondary de-bris shedding, if left unchecked, causes secondarydegenerative arthritis through a two-pronged pro-cess. It is a biologic process that attacks the phys-iologic function of the proteoglycans and eventually,the collagen; it is also a physical process that di-rectly abrades the hyaline cartilage surface, causingirreversible physical damage to the cartilage struc-ture, especially the collagen, that becomes the de-generative arthritis that disables the athlete. Thebiologic process alone can eventually reach the de-generative threshold after the collagen has been de-graded enzymatically or eroded physically becauseof a lack of adequate lubrication. But, the physicaldebris fragments stimulated by the healing responseof the parent bone are the most direct path to de-generation through the physical damage and thesecondary biologic response that they create. De-bris is the primary enemy of the athletic horse’sjoint.

7. Debris Management

Natural joint management of debris causes prioriti-zation of joint resources. In the normal situation,the synovial fluid is low in protein, contains almostno fibrin, and is viscous because of the large amountof hyaluronan within the joint.4 One purpose ofnormal synovial fluid is to lubricate all joint func-tions and promote decreased friction associated withjoint motion. It would be counterproductive, how-ever, to lubricate debris within the joint and encour-age it to repeatedly pass through the articulation.So, in an inflamed joint the lubricating capability ofthe joint is sacrificed temporarily for increases infibrin and reduction of joint motion to give the jointan opportunity to clear the offending debris. Whenthe insult is neutralized in the joint, the synovialfluid then returns to its normal highly lubricatingcapabilities. The need to remove debris is a com-mon occurrence in a normal joint.

It is clear, therefore, that allowing persistent de-bris shedding and low-grade inflammation withinthe joint is counterproductive in the long term, be-cause it compromises the joint’s ability to lubricateitself and maintain the articular cartilage in a wear-free state. The critical nature of maintaining thehyaline cartilage, because it cannot be reconstructedor replaced, points out the high priority that shouldbe placed on removing even low-grade chronic in-sults and normalizing the homeostatic lubricatingmechanism that preserves the hyaline cartilage.

When fragments of cartilage or bone are shedwithin the joint, the joint responds by producingfibrin. In the margins of the joint, this fibrin at-taches to the synovial villi and catches the debris asit circulates in the joint. The fibrin facilitates theattachment of the debris to the synovial villi forelimination. The debris is, therefore, removed frombearing surfaces of the joint, preventing it fromabrading the articular cartilage. The debris is se-questered in the cul-de-sacs of the joint. The tinygranulomatous nodules encasing the debris can of-ten be seen arthroscopically (Fig. 6). The fibrin andsmall nodules stabilize the debris so that the cellu-lar components, chiefly the neutrophils and macro-phages, can remove it.

Debris removal necessarily requires release of po-tentially destructive enzymes and free-radical mol-ecules as part of the process. When it occurs inshort bursts with acute insults, the process rapidlyclears the joint of debris and has little ill effect onthe articular cartilage and joint environment. It isbelieved there is not enough wear during a transientperiod of inflammation to do significant harm, but ifthe balance of production and degradation is shiftedtoward depletion of proteoglycan long enough to af-

Fig. 6. This intra-operative picture shows several fragmentsthat have been attached by fibrin to the synovial lining and arebeing encased by fibrous tissue (arrows). Note the vascular hy-pertrophy that is responding to the need for fragment removalfrom the joint cavity (arrowhead).


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fect cartilage lubrication, destruction of the cartilagesurface is initiated.

This rapid, efficient process of debris removalmakes it possible for the joint to respond to an acuteinsult such as surgery. If the joint were not able totolerate an acute insult, surgery would not be pos-sible. If the debris shedding is continuous, how-ever, then the continual enzyme liberation withinthe articular cavity affects not only the debris butalso the lubrication mechanisms of the joint and thenormal articular cartilage by progressive attrition ofthe proteoglycan content and loss of the normal lu-brication mechanism. This makes the articularcartilage vulnerable because it shifts the proteogly-can equilibrium (production equals destruction) to-ward destruction, resulting in proteoglycan loss.This compromises the articular cartilage lubricationmechanism, allowing surface wear and fibrillation tooccur. This causes normally physiologic loads togradually erode the layers of the normal hyalinecartilage, a permanent, progressive, and irreversibledegenerative change.

8. Surgical Treatment of Joint Injury

The role of surgery in the fetlock joint is simple:restore stability to facilitate primary bone healing orremove unstable fragments to prevent secondarybone healing. With few exceptions, surgery treatsbone disease, whereas surgery cannot “treat” arthritisthat is underway. If the arthritis is not beyond reso-lution, surgery can delay or mitigate the progressionby removing the inciting cause.37,38 Removal of frag-ments of traumatic or developmental origin keeps theparent bone normal and prevents the debris that doesmost of the damage. The horse performs on the re-maining normal joint surface. The restoration ofdamaged arthritic joint surfaces by surgical tech-niques remains a strongly pursued goal, but the “stateof the art” at this time is that it does not work verywell. The best chance for athletic function in a jointwith a fragment is to prevent the primary injury fromstimulating the process that degenerates the rest ofthe joint by removing the fragmentation and associ-ated debris. Joints with major cartilage loss in criti-cal areas remain career-damaging or career-endingchallenges. So, surgery is a better prevention than acure for arthritis with joint injuries in the horse.

9. Surgical Treatment: Do We Use It Enough?

Surgical treatment of joint fragmentation is rapidand effective in stopping debris being shed into thejoint. The removal of unstable bone and its associ-ated debris preserves normal joint surface that willbe lost if the parent bone attempts to heal an unsta-ble fragment. The process of the parent bone try-ing to reattach and heal an unstable fragment isoften worse than the primary disease. The extremerange of motion of the fetlock joint makes it evenmore vulnerable to this type of damage than mostother joints. Physical debris tends to disseminatethroughout the articular surface, scoring the carti-

lage surface until is sequesters in the cul-de-sacs ofthe joint (Fig. 7).

Any opportunity to interrupt this debris-sheddingprocess has a positive effect on a horse’s joint. Sur-gery should be used more often and earlier than weoften elect to treat articular injury before it doesirreversible damage.

The strategy in treating traumatic and develop-mental joint injury is to negate the inciting andperpetuating cause, usually an unstable or mal-formed area of joint surface, and preserve every bitof normal joint architecture and hyaline cartilagepossible. Surgical stabilization or surgical removalof the problem, whenever possible, is the most de-finitive treatment and results in the fastest, bestresolution of the problem. In most instances,modifying the clinical signs medically, without elim-inating the perpetuating physical cause, risks per-manent damage.

10. Examination and Treatment of Traumatic andDevelopmental Diseases of the Fetlock Joint

Categorizing and Staging Fetlock Joint Inflammation andIts TreatmentIt is useful during the examination of an injuredjoint to categorize the disease. When one evaluatesthe radiographs of a joint, it is imperative to assessthe health of the joint in light of whether or not theperpetuating cause can be removed and the jointpreserved. Localized reaction to an insult (focal ly-sis and proliferation in an area of fragmentation orfracture and excess synovial fluid without signifi-cant fibrous thickening) carries a better prognosisthan a generalized reaction (marginal spurring atmultiple sites, thinning of articular cartilage, andfibrous thickening). The localized reaction is anindication of the parent bone trying to stabilize the

Fig. 7. This intra-operative view of the dorsal proximal jointspace of the fetlock joint shows debris that is free in the joint(arrow) and attached and fibrosed into the synovial lining(arrowhead).


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fragment. Generalized reaction is an indication ofchronic disease and irreversible injury from achronic insult. Localized reaction is often amena-ble to resolution surgically. Generalized reaction isindicative of permanent change.

Radiographic Markers of Previous Inflammation in theFetlock JointThere are two easily discernable radiographic mark-ers of previous severe inflammation of the fetlockjoint. Even when previous severe inflammation isresolved, if either one of these markers is present, itindicates that the horse’s athletic career has beencompromised. The first is sesamoiditis, indicatedby the enlargement and change in shape of the vas-cular canals of the sesamoid bone. This is a markerfor injury to the suspensory ligament insertion andoccurs after serious inflammation of the sesamoidbone, usually because of trauma, and possibly, pre-vious fracture of the sesamoid bone. This enlarge-ment and change in shape of the vascular canals isan indication of reduced career performance.39

The second marker is supracondylar lysis, whichresults from chronic inflammation of the synoviallining on the palmar distal aspect of the cannon boneabove the articular surface. This radiographicfinding is a non-specific indicator of previous severeinflammation of any kind within the fetlock joint.If supracondylar lysis is present, it indicates thatsome serious previous disease such as septic arthri-tis, fracture, or other severe trauma was previouslypresent. The presence of supracondylar lysis hasbeen documented as a marker of decreased perfor-mance in the horse.40,41 However, it is likely notthe supracondylar lysis itself that is the problem butrather the disease that previously created the severeinflammation and supracondylar lysis that is of con-cern. Supracondylar lysis indicates the need for

investigation and assessment of the previous severedisease and its effect on the fetlock joint.

Forelimb Versus Hindlimb Fetlock Joint AnatomicDifferencesThe osseous anatomy of the forelimb and hindlimbfetlock joints is similar; but the ligamentous anat-omy is different. The fetlock joint moves in onlyone plane—sagittal. Motions in other planes play arole in many fetlock joint injuries. The ligamen-tous support in the forelimb is placed more dorsal,preventing hyperflexion that separates the dorsalarticular margins and providing much more resis-tance to torsion forces. The ligamentous support inthe hindlimb is more plantarly placed on the medialand lateral aspects of the fetlock joint, which allowsthe dorsal articular margin to hinge open in hyper-flexion. The collateral ligaments provide much lessresistance to torsion, especially in the non—weight-bearing position (Fig. 8).

During weight bearing, the sagittal ridge of thecannon bone and the sagittal groove of the firstphalanx and intersesamoidean ligament provide theprimary resistance to torsion. When torsion is ap-plied in the partially weight-bearing or non—weight-bearing positions, it is the ligamentoussupport that resists the torsion and determineswhere an injury will occur. The different anatomymakes this different in the forelimb and the hind-limb. Torsion damage is much more common in thejuvenile animal than the adult, because the bone isstill growing and failure at sites of bone growth ismore common because of their reduced strength.42

Injuries in torsion occur primarily in the non-weighted position. In the forelimb, in contrast tothe hindlimb, the collateral ligaments maintain thearticular surfaces in apposition when the first pha-lanx is twisted. This causes the sagittal ridge to

Fig. 8. Two radiographs show the difference between the collateral ligament restriction during maximum flexion in the forelimb (left)and the hindlimb (right).


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remain firmly apposed to the dorso-medial anddorso-lateral eminences of the first phalanx whenthe fetlock joint is flexed, and disturbances in boneformation occur commonly in the distal sagittalridge in the forelimb where the resistance to thetorsion occurs. The medial or lateral dorsal emi-nences of the first phalanx can also suffer damage inthe resistance to torsion. This damage results inthe occasional chip fracture of an eminence as aresult of this trauma. The resistance of the sagittalridge and grooves to torsion provides some protec-tion to the palmar ligamentous attachments of thefetlock joint in the forelimb, so although palmar firstphalanx avulsion fragmentation at the attachmentsof the distal sesamoidean ligaments occurs, it is notnearly as frequent as in the hindlimb.

In the hindlimb, the caudally placed collateralligaments allow the dorsal aspect of the joint tosubluxate in the non—weight-bearing position whentorsion is applied. As this occurs, fragments arecommonly created from the axial aspect of the me-dial or occasionally, the lateral dorsal eminence ofthe first phalanx. The distal sagittal ridge is rarelydamaged in the hindlimb because of this disarticu-lation. The disarticulation allows the torsion toproceed until the caudal ligamentous support re-sists. As it resists in the growing horse, the site ofgrowth is the weakest link, and fragments of grow-ing bone are pulled free at the ligamentous attach-ments of the distal sesamoidean ligaments andcollateral ligaments, resulting in plantar P-I frag-ments much more commonly in the hind fetlock thanin the fore fetlock. These anatomic differences re-sult in marked differences in incidence of the vari-ous juvenile bone injuries in the forelimbs andhindlimbs of the horse.

11. Serous Arthritis

Distention of the joint capsule by synovial fluid with-out radiographic signs was formerly classified as adisease category in and of itself. Newer diagnosticmethods including arthroscopic surgery, magneticresonance imaging (MRI), and digital radiographyas well as better targeted radiographic positioningand improved understanding of the disease pro-cesses now cast doubt on whether or not this is a realcondition. It is likely that almost all cases of serousarthritis have an underlying pathologic injury.It may be that the pathologic injury is simply aninsult to the soft tissues or a comparable insult tothe bone that is below the level of radiographic de-tection, but it is likely there is a pathologic cause forall cases of synovial distention.

The distention of the joint capsule with poor-qual-ity synovial fluid and its concomitant sacrifice of thelubricating mechanism in the interest of the moreurgent need for removal or healing of the offendinginsult results in synovial distention with a lack ofradiographic findings. The excess synovial fluidproduction is a response to some thing. Chronicoveruse can be a cause of serous arthritis with min-

imal radiographic changes as the articular cartilagebegins to suffer superficial loss of cartilage structurewith fibrillation, but this is usually present in mul-tiple or paired joints with a minimally progressivecourse. This is a prime indication for disease-mod-ifying medical therapy to support the joint functionbut denotes caution with symptom-modifying medi-cation that could contribute to the progression of theproblem.13

Acute onset single-joint serous arthritis normallyhas a pathologic cause. Current diagnostic imag-ing capability is identifying a cause for most of thesecases. Many of these are lesser versions of well-known injuries, and some can benefit from surgicalor medical treatment.

12. Diseases of the Distal McIII/MtIII First PhalanxArticulation

Osselets (Little Bones) or Capsular Insertion Inflammation

Osselets were formerly, and are occasionally still, anoccupational hazard of most horses that work atpower or speed.43 If horses race or work longenough, their fetlock joints enlarge because of a myr-iad of reasons causing inflammation. These causesare now generally separated and treated as individ-ual diseases. The basic pathology of the condition,hypertrophic proliferation of the dorsal capsular in-sertions, is caused by any cause of inflammationchronically present in the dorsal fetlock joint.44

Most commonly incriminated are hyperextensionand the impact trauma of the dorsal aspect of thehyperextended first phalanx on the dorsal cannonbone.43,45 This occurs primarily in the fore-limb.45,46 Chronic damage and the resultant in-flammation cause softening of the bone where thecapsule inserts both on the first phalanx and on thedistal cannon bone. Fragmentation will also con-tribute to the softening of the bone through its heal-ing response to fragments. As the “Sharpey’sFibers” of the capsular insertion begin to lose theiranchorage in the softened bone, they begin to pullfree. This results in inflammation of the fetlockjoint capsule or capsulitis.47 The bone proliferatesand the capsule thickens in an attempt to reinforcethe lost capsule insertion by hypertrophy, and therange of motion of the joint decreases.

The loss of capsule anchorage becomes a self-per-petuating disease with fetlock use pulling more fi-bers free from the bone; this causes moreinflammation and further weakening of the fiberinsertion, resulting in cyclic fiber damage. Fibroustissue proliferation and thickening of the joint cap-sule reduces the flexibility of the capsule, whichincreases the extraction forces on the capsule fibers,because the fetlock joint capsule will no longer foldwith flexion. This further pulls on the insertionbecause of the loss of flexibility, further contributingto the damage and fibrosis and perpetuating thecycle. Instead of pain-free motion, the stiffenedjoint capsule creates yet more thickening. Bone


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and soft-tissue proliferation occur as the insult tothe capsule insertion progresses until, in somehorses, the stiffness becomes so prominent that jointflexion becomes almost impossible. Before routineradiography, if a disabled thickened fetlock jointwas examined during a post-mortem examination, itwould often reveal mineralization within the fibro-sis; these “little bones” within the joint capsulesgave rise to the name osselets (Fig. 9).

With the advent of digital radiography and morefrequent use of arthroscopic surgery for early re-moval of dorsal P-I fragments, the most commoncause of osselets is now routinely resolved early inthe course of the disease, circumventing the bonesoftening and capsular thickening that is the resultof chronic dorsal first phalanx fragmentation. How-ever, if fibrosis of the joint capsule is promoted fromany cause, it can become the self-perpetuating chroniccapsular thickening. If dorsal fetlock joint capsularthickening occurs without radiographic changes of thebone, it is commonly referred to as a green osselet, butradiographic inflammation of the bones is commonand commonly identified.

Fibrous capsular proliferation can be limited earlyby identifying and treating the primary disease suchas dorsal P-I fragmentation. Combined with a pe-riod of reduced exercise, treatment will often pre-vent the marked capsular thickening that followsthe chronic inflammation.

The classic treatment for osselets was therapeuticcautery, which historically seemed to be surpris-

ingly useful in some instances.48 Some people feelthat the principal treatment is the time away fromtraining that accompanies the therapeutic cautery,but time alone seldom achieved a similar response.48

More recently, shockwave therapy is being used inthe treatment of the capsular insertion inflamma-tion, and capsular insertion inflammation seems torespond to the shockwave treatment, often allowingcontinuation of training.49 However, in my experi-ence, continued training combined with the analge-sia of the shockwave therapy sometimes encouragesthickening that results from this progressive dis-ease. The most successful approach to the preven-tion of permanent disability resulting from jointcapsule thickening remains the elimination of theprimary cause of the capsule inflammation, such asdorsal P-I fragmentation, when possible. Similarto degeneration of the articular cartilage, the pro-gressive thickening of the dorsal joint capsule of thefetlock has a threshold beyond which it becomesself-perpetuating (Fig. 10). If capsular thickeninghas progressed to the point that it eliminates theflexibility of the dorsal joint capsule, removal of aninciting cause such as dorsal P-I fragmentation nolonger halts the progression.

Exostosis of the Lateral Digital Extensor Tendon Insertionon P-IAn exostosis of the lateral digital extensor tendonwill occasionally occur on the dorso-lateral proximalfirst phalanx just below the joint capsule insertionon the first phalanx where the lateral digital extensorinserts on the first phalanx. This is often confused

Fig. 9. This radiograph shows chronic joint capsule thickening(double arrow) or osselets with joint capsule mineralization (ar-rowhead).

Fig. 10. This picture of a right front fetlock joint shows thechronic dorsal joint capsule enlargement of osselets (arrow).


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with fetlock joint capsular insertion inflammation butis a distinctly different injury. The thickening withproliferation of the insertion of the lateral digitalextensor tendon is prominent clinically and radio-graphically, but it occurs only laterally on the firstphalanx in contrast to true capsular insertion in-flammation that occurs across the entire dorsal firstphalanx. Lateral digital extensor insertion inflam-mation is located immediately distal to the capsuleof the fetlock joint rather than at the capsule inser-tion (Fig. 11).

Although the reaction is prominent and the enthe-siophytes that are produced are impressive, the re-action is accompanied only by mild transientlameness, if there is any lameness at all. This pro-liferation is cosmetic only and does not require treat-ment. It has an excellent prognosis for futuresoundness and only requires attention if the cos-metic lump is a concern, in which case restriction ofexercise until the inflammation subsides isrecommended.

Dorsal P-I Chip Fractures in the Adult HorseChip fractures of the proximal aspect of the firstphalanx on the dorsal articular margin are commonin racing horses but are also found in horses of otheruses.11,50 The biomechanics of creation in the adulthorse are principally hyperextension of the fetlockjoint with the first phalanx dorsal rim impacting onthe cranial aspect of the metacarpus/metatarsus atthe dorsal proximal fetlock joint margin.51 Thisimpact is implicated in several pathologic conditionsrelated to the hyperextension including ulceration of

the dorsal proximal articular surface of the distalmetacarpus/metatarsus, villonodular synovitis, anddorsal joint capsule thickening as well as the frag-mentation and ulceration of the proximal aspect ofthe first phalanx. These conditions will occasion-ally occur in the hindlimb but are much more com-mon in the forelimb where the most weight is born inthe adult horse. Fractures occur more commonlyon the medial eminence than the lateral eminencewhen uniaxial, but biaxial (medial and lateral to thesagittal groove) fragments are common. The frag-mentation with cartilage ulceration occurs primarilyon the abaxial margin of the eminence in the adulthorse.

The fragments are created, in most instances, byrepeated impact with eventual structural damage tothe bone as a result of the repeated trauma, and

Fig. 12. This intra-operative view of the dorsal first phalanx(right) shows the dorsal first phalanx chip fracture (bracket) thatis shedding the debris that is scoring the distal metacarpus (left)(arrowheads).

Fig. 13. This radiograph shows a subacute P-I chip (arrow)fracture with accompanying bone demineralization at the inter-face of the fragment with the parent bone (arrowhead).

Fig. 11. This radiograph shows a chronic lateral digital extensorexostosis.


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then separation of the bony fragments (Fig. 12).The impact damage as well as the presence of thebony fragments and the bone healing responses thatthey create result in debris shedding into the joint,inflammation, and pain (Fig. 13). Pain also resultsfrom the invasion of the chip fracture/inflammationcomplex into the sensitive joint capsule insertions onthe dorsal aspect of the first phalanx if the diseaseprocess progresses deep enough into the bone of thedorsal margin of the first phalanx to affect the cap-sule insertion. During hyperextension and impactof the chip fracture on the distal cannon bone, thefragments are pushed forward and invade the jointcapsule attachments if the fragments are large.Joint capsule fibers also become involved with thegradually softening of the bone of the proximal firstphalanx by means of the gap-strain healing re-sponse that is created by all unstable fragments ofbone. Softening of the bone then allows for avul-sion of the capsule fibers in the process that createsthe primary dorsal joint-capsule thickening diseasedescribed previously.

The simplest, fastest, and best treatment for dor-sal P-I fragmentation is arthroscopic removal.11,50,52

This results in the best and fastest possible resolu-tion of the pain and lameness caused by the dorsalP-I chip fractures. Given a prolonged period ofrest, some horses will be able to heal a dorsal P-Ichip fracture, but they usually heal with a moreprominent dorsal margin on the first phalanx com-pared with normal, making reoccurrence of the im-pact of the first phalanx on the distal cannon boneeven more likely than before injury.

Some horses are able to create a pseudo-arthrosisbetween the chip fracture and the parent bone byhealing the raw bone surfaces with fibro-cartilage(Figs. 14 and 15), and for lower level exercise, this isa functional solution for the problem.53 But, in ath-

letic horses, the fibro-cartilage rarely survives heavyuse, and as the fibro-cartilage wears through andraw bone is again exposed, the debris shedding pro-cess is reinitiated. So, for most heavy-use horses,the only lasting solution to the problem is surgicalremoval of the fragmentation.

The clinical signs can be transiently mitigatedwith intra-articular medication, but this creates thedual toll on the interior of the joint of stopping theinflammatory response that neutralizes the debrisbeing shed into the joint and compromising the ar-ticular cartilage’s ability to lubricate itself and pre-vent the wear that occurs on normal weightbearing.4 So, this is a transient rather than a long-term solution.

Surgical removal and debridement of the debrisare effective and rapid ways to resolve the detrimen-tal effects of a chip fracture on the dorsal aspect ofthe first phalanx. It is one of the most common andmost successful surgeries in the fetlock joint and canreturn the joint to normal after surgery if treatmentis undertaken early in the disease process.11,50

Dorsal P-I Chip Fractures in the Juvenile HorseChip fractures in the juvenile horse are more com-mon in the hindlimb than they are in the forelimb.This seems to be caused by the biomechanically dif-ferent forelimb and hindlimb action. In the hind-limb, the chip fracture in the juvenile horse iscreated by torsion force separating a fragment ofgrowing bone from the parent bone at the interfaceof the first phalanx and the sagittal ridge of thedistal cannon bone. The location of the chip frac-ture is more axial than in the adult, where the chipfracture most often occurs on the abaxial margin ofthe dorso-medial or dorso-lateral eminence.

The chip fracture will initially be quite small ra-diographically, but as the horse grows and the sep-arated fragment fully ossifies, it is much larger thanit appears initially. The fragment is initially sepa-rated from its vasculature but normally regains vas-culature with continued growth and healing, and inmany instances, it reattaches to the first phalanx.

Fig. 14. This radiograph shows a chronic P-I chip fracture (ar-row) that has developed a fibrous pseudo-arthrosis between thechip fracture and the parent bone.

Fig. 15. This intra-operative view shows the fibro-cartilage in-terface (arrows) between the chip (top left) and the first phalanx(bottom); the distal cannon bone is on the right.


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However, it often alters the contour of the dorsalaspect of the first phalanx and creates a prominencethat, on initiation of high-speed exercise, is im-pacted on the distal cannon bone and detaches againfrom the parent bone. Therefore, the prominenceincreases the risk for chip fracture and is extremelyvulnerable to high-speed or heavy exercise. Whenit is again separated from the parent bone, it reini-tiates all of the problems free fragments createwithin the joint.

There has been some debate as to whether or notthese fragments need removal; however, examina-tion of racing performance with these fragments inthe joint show that they detrimentally alter thehorses’ performances.41 Surgical removal is advis-able for elimination of the debris shedding and thecycle of inflammatory degradation of the joint thatoccurs.11

Proximal Dorsal Fetlock Articular Surface ErosionDuring hyperextension, the proximal phalanx im-pacts the distal cannon bone just above the articularsurface. It can have one of many results includingchip fractures of the first phalanx, frontal planefractures of the first phalanx, villonodular synovitis,dorsal joint capsule thickening, or simple erosion ofthe subchondral bone of the cannon bone proximalarticular fetlock joint surface (Fig. 16). Often, com-binations of these diseases will occur, but the ero-sion at the top of the articular surface that resultsfrom impact during hyperextension commonly ac-companies dorsal fragmentation of the first phalanx.

This erosion of the cannon bone sheds debris; inthe author’s experience, this by itself is not a major

source of debris and subsequent inflammation, be-cause there are rarely separated bone fragmentsthat initiate a healing response to accompany thedirect trauma. Primary treatment of the other con-ditions accompanying this surface erosion is likely toresolve the problem. So, as a disease condition, thecannon bone remodeling is mostly a sign of otherarticular pathology and radiographically appears tobe related to the severity of the damage in the joint.

When found accompanying other injuries, theproximal articular surface of the metacarpal condyleerosion is debrided of loose fragmentation, but ag-gressive curettage and invasion of the joint capsuleattachments just proximal to the erosion is counter-productive in returning the joint to soundness.

Dorsal Synovial-Pad Thickening (Villonodular Synovitis)

Villonodular synovitis, more correctly termed dorsalsynovial-pad thickening, is an overdiagnosed condi-tion. The description villonodular synovitis is anadaptation from human medicine that is slightlyinaccurate but denotes pathologic enlargement ofthe normal synovial fold at the proximal aspect ofthe articular surface in the dorsal compartment ofthe fetlock joint.54,55 Hyperextension trauma ac-counts for many diseases in the dorsal compartmentand is responsible for this disease. If the first pha-lanx traumatizes the synovial fold at the top of thearticular surface between itself and the distal can-non bone during hyperextension, the synovial foldbegins to swell and enlarge (Fig. 17). Calcificationwithin the fold has been described.56

Fig. 16. This radiograph shows dorsal proximal articular sur-face erosion (bracket) caused by hyperextension and impact dam-age.

Fig. 17. This radiograph of a contrast arthrogram of a fetlockjoint illustrates the presence of an enlarged dorsal synovial pad ofthe fetlock joint (arrow).


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The fold enlarges by the deposition of fibrin on itssurface. As in any wound, fibrin gradually convertsto granulation tissue and eventually fibrous tissue,thickening the fold in the process. If the synovialfold enlarges enough, it begins to encourage addi-tional trauma by its size, and the process becomescyclic with enlargement creating additional traumaand additional trauma creating enlargement. Trueequine villonodular synovitis involves enlargementof the villonodular pad alone with no thickening ofthe joint capsule and relatively little other diseasewithin the dorsal compartment. When the synovialpad becomes large enough, a smooth erosion of thedorsal cortex occurs from the cyclic direct pressureon the bone.

The confusion in diagnosis comes from the syno-vial-fold enlargement, which occurs with any dorsalcompartment pathology when all of the dorsal softtissues of the dorsal fetlock joint begin to enlarge.56

This includes osselets, thickening of the dorsal jointcapsule, dorsal P-I chip fractures, and proximal ar-ticular surface ulceration. Only when the joint isnormal except for an enlarged synovial fold andthere is no additional pathology is the term vil-lonodular synovitis or synovial-pad thickening ap-propriate. If true villonodular synovitis is present,it can often be detected with ultrasound examina-tion of the dorsal compartment of the joint; however,ultrasound is sometimes unable to separate thick-ening from the villonodular pad or the joint cap-sule.57 The most diagnostic examination is acontrast arthrogram, which will most accuratelyshow enlargement of the villonodular pad.

Ulceration of the top of the articular surface withno enlargement of the villonodular pad is commonlymisdiagnosed as villonodular synovitis by veterinar-ians when there is no thickening of the dorsal syno-vial fold or simply thickening of the joint capsule.Hyperextension trauma of the dorsal aspect of thefirst phalanx impacting on the distal cannon bonecreates traumatic ulceration and demineralizationin a similar location but usually just distal to thetrue villonodular pad erosion above the articularsurface, and the dorsal articular surface ulcerationis normally not well delineated and is not smooth incontour as is the pressure-induced erosion of vil-lonodular synovitis.

In the author’s experience, any disease of thedorsal compartment that creates inflammationcan create thickening of the villonodular pad aswell as the other soft tissues of the joint. Part ofany arthroscopic procedure to remove other pa-thology involves villonodular pad examination andsurgical reduction as necessary. Treatment ofthe primary disease and reduction of the inflam-mation in the dorsal compartment will result inregression of the edema of the villonodular padcaused by those diseases. However, if true fi-brous thickening occurs, then arthroscopic re-moval of the villonodular pad is the treatment ofchoice. Intra-articular medication can reduce the

size of the villonodular pad and the secondarythickening that accompanies other diseases, butthis is not true with villonodular synovitis wherethickening of the pad is caused by fibrosis.

The prognosis is favorable for resolution of lame-ness as well as normal anatomy of the dorsal fetlockwith arthroscopic removal of the villonodular pad, ifit is the primary condition.57 In conditions wherethe pad is thickened secondary to another primarydisease, it is the primary disease that determinesthe prognosis.

Frontal Plane P-I Fractures

Frontal plane P-I fractures occur in a plane par-allel with the dorsal cortex of the first phalanx atthe proximal articular surface of the first pha-lanx.58 These fractures occur more commonly inthe hindlimb than the forelimb and can occur me-dially or laterally. Larger fractures involve themedial and lateral dorsal eminences of the firstphalanx. The size varies from small fragmentsthat are similar to dorsal first phalanx chip frac-tures to the very large biarticular fractures thatbisect the first phalanx, affecting both the fetlockand pastern joints (Fig. 18).

Chronic hyperextension and impaction of the firstphalanx onto the dorsal surface of the distal cannonbone is the mechanism for creating this fracture.The fractures are found in all degrees of completionfrom just a fine fissure at the articular surface tocomplete and unstable fractures; this is highly sug-gestive of stress-fracture formation with propaga-tion of varying degrees.

The very small fragments are unstable, similar inall aspects to the more common chip fractures in thetransverse plane, and should be treated with re-moval similar to those fractures.

The intermediate-sized fractures involve only oneeminence of the dorsal P-I and are almost alwaysstable at less than high-speed exercise, because theyare stabilized across their entire face by the fetlockjoint capsule attachment and do not enter the jointdeep enough into the articular surface to be unstablein normal weight bearing. If the exercise level isreduced, the fractures heal well without interven-tion or internal fixation because of the large stablejoint capsule attachment. Interestingly, in the au-thor’s experience, the fractures are sometimespresent for some time and are well into the healingprocess before they cause enough lameness to limitperformance. They are also frequently bilateral,occurring simultaneously in both hindlimbs or bothforelimbs. Removal from training results in reduc-tion in biomechanical strain and allows healing inmost intermediate-sized fractures.

The large fractures are deep enough into the ar-ticular surface that they are unstable at rest or withsimple walking exercise. In large fractures, weightbearing causes the round distal articular surface ofthe cannon bone to separate the dorsal and plantararticular surface components. The approach to this


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fracture must be internal fixation to preserve thearticular surface using techniques similar to thesagittal version of the first phalanx fracture but inthe frontal plane.

Distal McIII/MtIII Sagittal Ridge OCD

A proximal sagittal ridge OCD is a frequent occur-rence in any of the four fetlocks in horses.59 Thisjuvenile disease, like most other forms of OCD, re-sults from trauma to developing bone. Proximalsagittal ridge OCD has been categorized based onthe reaction of the subchondral bone and the pres-ence of a fragment.60 A simple defect in the sub-chondral bone without clinical signs is of littleconsequence. A defect in the subchondral bonewith associated inflammation in the bone is of con-cern, but unless a fragment develops and is visibleradiographically, there is a good chance of sponta-neous resolution.

If a fragment develops in the area of inflamma-tion, then it is important to remove the osseouslesion if the inflammation persists. As with chipfractures, small bone fragments can be surroundedby fibrous tissue and fibro-cartilage and can becomequiescent; also like chip fractures, the interface offibro-cartilage is vulnerable to high-speed exercise.Fibro-cartilage is vulnerable to erosion, causing an-other intrusion into the subchondral bone, initiatingsecondary bone healing response and debris shed-ding, and reinitiating inflammation and chronic de-generation within the joint. Radiographs generallyunderestimate the size of an OCD fragment at theproximal aspect of the sagittal ridge (Fig. 19). Thecartilaginous fragment is only partially ossified inthe immature horse, and the cartilaginous dimen-sions are much larger than the radiographic osseousfragment. Continued growth and maturation en-larges the proximal sagittal ridge OCD fragment,thins the cartilage cover as the fragment maturesand the bone further ossifies, and increases thechances that a bone-to-bone interaction will be ini-tiated to try and heal the fracture.

In the author’s experience, the severity of jointinflammation caused by OCD lesions of the top ofthe sagittal ridge in the fetlock is directly related totheir ability to shed debris within the joint and isrelated to the size of the fragment and its bone-to-bone interface. If synovial effusion and clinicalsigns are persistent either at the time of the devel-opment of the OCD or appear later in the horse’scareer, surgical removal is indicated. If the joint istotally quiescent, monitoring may be all that isneeded, and if clinical signs occur, then surgicalremoval would be the treatment of choice. Theprobability of clinical signs is related to the size ofthe lesion, location, and intended use of the horse.A small lesion in a horse intended for moderatelystressful use is unlikely to ever cause a problem.A similar lesion in a horse intended for highlystressful activity might cause chronic low-grade in-flammation and eventually, joint degeneration thataffects performance. Large lesions will likely sheddebris and become problematic for most horses.Symptom-modifying medication warrants cautionand monitoring for ongoing degeneration. Surgical

Fig. 18. (A) The first radiograph shows a small frontal planefracture that is best removed. (B) The second radiograph showsa moderately sized frontal plane fracture that requires no treat-ment, only removal from exercise, and (C) the third radiographshows a biarticular frontal plane P-I fracture.


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removal with debridement of the parent bone is aroutine arthroscopic procedure in the dorsal aspectof the fetlock joint and is one of the most straight-forward arthroscopic procedures undertaken.

Occasionally, an OCD lesion will occur in the cau-dal aspect of the joint at the very proximal aspect ofthe sagittal ridge, but its treatment is no differentthan the OCD lesions of the proximal sagittal ridgein the dorsal compartment.

An OCD of the distal sagittal ridge OCD in theforelimb is a different situation from the proximalsagittal ridge OCD fragment. This lesion variesfrom a few millimeters to over one centimeter in sizeand is visible on the flexed lateral and the dorso-palmar (D-P) radiographic views (Fig. 20).

This OCD lesion occurs only in the forelimb, isprimarily a non-ossified area of joint surface involv-ing the distal sagittal ridge, and is rarely accompa-

nied by a separated osseous fragment. It is theresult of disruption of the interface between thecalcified cartilage and subchondral bone at the baseof the sagittal ridge and is centered �2 cm below thetop of the ridge (Fig. 20). The lesion results from atorsion force by the first phalanx loading the sagittalridge perpendicular to the ridge and parallel to thearticular surface of the condyles. Torsion in theforelimb, which causes the sagittal ridge to receivepressure from the medial or lateral eminence of thefirst phalanx because of the collateral ligament’srestriction of motion, results in damage to the grow-ing bone at the base of the sagittal ridge. Thetrauma results in cleavage between the calcified car-tilage and the subchondral bone and is a differentversion of OCD than is commonly seen in the horse(Fig. 21).

The lesion is more like OCD frequently seen in thehuman juvenile male where the cleft is through the

Fig. 19. This radiograph illustrates a proximal sagittal ridge OCD with a separated fragment. The picture shows the gross size ofthe fragment.

Fig. 20. This radiograph shows a distal sagittal ridge OCD(bracket).

Fig. 21. This intra-operative picture of a distal sagittal ridgeOCD shows the plane of detachment (arrow), which is under thecalcified growth cartilage. The calcified cartilage is still at-tached to the articular hyaline cartilage (arrowhead).


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superficial layers of bone rather than through theinterface of cartilage and bone, like in most in-stances in the horse. The difference in the diseaseis that the ability of the parent bone to reattachcalcified cartilage is far superior to the virtual in-ability to reattach cartilage to bone as with mostOCD seen in the horse. With distal sagittal ridgeOCD lesions, the cleft will heal in nearly all in-stances unless the lesion is disrupted, displaced, andunstable.

After the interface between the calcified cartilageand parent bone is bridged, normal maturation ofthe cartilage can occur, and the distal sagittal ridgeOCD matures, resolving the radiographic defect.If a fragment separates, there is severe synovialeffusion and lameness. Unless synovial effusion orlameness is present, distal sagittal ridge OCD le-sions are normally not treated but just monitored.If clinical signs are apparent, then arthroscopic re-moval is necessary.

The difficulty with arthroscopic removal of thislesion is that it leaves a large deficit in the sagittalridge and the radiographic appearance of the joint ismarkedly altered. Although it has little effect onthe joint’s function and the prognosis for soundnessis good, if the horse is ever considered for purchase,it often creates considerable concern because of thestark change in radiographic appearance caused byremoval of the distal sagittal ridge.

The prognosis after removal of sagittal ridge OCDlesions is favorable if the lesions are confined to theridge. If the lesions spread onto the condyles, theprognosis worsens proportional to the amount ofjoint surface lost. The biggest risk from a sagittalridge OCD is a decision to leave it in situ when it isshedding debris. If the articular surface is irrepa-rably damaged removal of the OCD no longer hasany benefit. The damage done to the articular sur-face by the shedding debris is permanent, and thehyaline cartilage lost is irreplaceable. So, if persis-tent effusion is present, damage is being done to thejoint, and without removal, the articular cartilage isbeing lost. When this lesion separates, the debris

shedding is significant, so the synovial effusion andlameness is significant as well, indicating the ag-gressive ongoing damage to the joint surfaces.

13. OCD Lesions of the Dorso-Medial or Dorso-Lateral Margin of McIII/MtIII

OCD lesions of the dorsal margins of the cannonbone can occur in forelimbs or hindlimbs. Torsionof the joint stretches the joint capsule attachment tothe abaxial margin of the cannon bone, resulting inthe avulsion of a portion of the growing bone. (Fig.22).

These fragments will sometimes heal, but if afragment is present, the effect is similar to a frag-ment at the top of the sagittal ridge. Small frag-ments in this location are frequently innocuous; butif they are large enough to incite the secondary bonehealing response that results in debris shedding intothe joint, they are indications for arthroscopic re-moval similar to other fragments. Also, similar toother fragments, size of the fragment and use of thehorse are factors, but if the fragment generates sy-novial effusion, it is an indication that it is sheddingdebris into the joint and is best removed to protectthe joint if the horse’s career warrants.

14. OCD

Lesions of the Distal Metacarpal or Metatarsal Condyles

OCD lesions of the distal metacarpal or metatarsalcondyles are normally found in the neonate and areoften associated with foals that have other delayeddevelopment diseases. They can be painful butrarely form a true dessicans lesion. Therefore, os-teochondrosis, which indicates delayed develop-ment, is likely a more appropriate term thanosteochondritis dessicans. The lesions are morecommon on the more cranial aspect of the cannonbone articulation with the first phalanx, althoughthey can occasionally occur on the palmar or plantararticulation with the sesamoid bone (Fig. 23).

In most horses, the osteochondrosis lesion ma-tures and disappears with time. Depending on the

Fig. 22. This radiograph illustrates a margin OCD of the distal McIII condyle (arrow), and the intra-operative picture shows the samefragment (bracket).


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size of the lesion, restriction of activity may beneeded. Large lesions are weak compared withnormal bone and may cause lameness with exercise.Rarely, a true flap-like dessicans forms and requiresremoval. If this occurs in the dorsal articulationwith the first phalanx, this is a straightforward ar-throscopic procedure, if the cartilage flap is small.On occasion, a large flap involving much of the con-dyle develops; these are career limiting and are theprinciple concern when a distal cannon bone osteo-chondrosis is found. Because these lesions are solarge that the damage is irreversible by removalafter they develop, restricted exercise is recom-mended until the distal cannon bone matures.

More commonly, the thickened weakened articu-lar surface will crack, and a subchondral bone cyst ofthe distal cannon bone will form. If the cyst per-sists, then it must be dealt with surgically.

Osteochondrosis lesions of the palmar/plantarcannon bone articulation with the sesamoid bonesare normally less extensive and normally resolvewith time, but the same concerns with size and thepossibility of cartilage separation apply in this loca-tion as well; so, monitoring the size of the lesion andthe maturation in relation to the amount of exercisestress is appropriate.

Confusingly, the palmar distal cannon bone de-generation of the racehorse has been termed OCD insome reports. This degeneration is a traumatic le-sion related to the stress of high-speed exercise andis not related to the developmental disease that wenormally call OCD. Preferentially, we should keepthese two conditions separated in terminology andrefer only to the developmental disease as OCD.

Distal Metacarpal/Metatarsal CystsCystic lesions of the distal aspect of the cannon bonebegin as osteochondrosis lesions on the condyles ofthe distal cannon bone. They are normally found inthe metacarpus.61 These cysts are frequently bi-axial. Osteochondrosis lesions of the condyles fre-quently improve with time, become ossified, andheal, remodeling into the parent bone. However, as

long as the thickened articular cartilage persists,the articular surface is vulnerable to trauma.

If trauma creates a crack in the abnormal carti-lage of the articular surface, synovial fluid can bepushed through the slit into the subchondral bone.The subchondral bone will begin to form a cysticcavity in response to the cyclic pressurization. Cyc-lic loading causes intermittent pressurization of thecystic cavity with the synovial fluid being pushedinto the subchondral bone with each weight-bearingstride, causing the bone to reabsorb and form thecyst. The cyst will enlarge until it becomes largeenough that the amount of synovial fluid that ispushed through the slit in the articular surface is nolonger sufficient to increase the pressure within thecystic cavity; then, a sclerotic border forms aroundthe cyst as pressure equalizes and the bone attemptsto remodel and neutralize the cyst and its biome-chanical effect on the bone (Fig. 24).

The inflammation associated with the active for-mation of the cyst often causes pain and lameness asdoes the increased pressure within the bone thatresults from the pushing of synovial fluid into thecyst on weight bearing. Distal McIII cysts often getto a steady pain-free state with time; on increases inthe horse’s level of activity, the pressure may in-crease, and the cyst may again become reactive andpainful to the horse, creating lameness. Therefore,as long as the slit-like defect in the articular surfacepersists, the danger of lameness from a cyst persistsas well.

Cysts almost always form on concave/convex ar-ticular surfaces, because the shape of the articularsurface facilitates the pressurization of the joint sur-face on weight bearing, forcing synovial fluid intothe subchondral bone.62 Therefore, the cysts ofconcern are usually on the condyles.

The treatment for subchondral cysts requires achange in the joint-surface biomechanics to inter-rupt the pressurization of the cyst. The most effec-tive treatment is the removal of the OCD lesion thatpredisposed the articular surface to forming a cystic

Fig. 23. This (left) is the intra-operative picture of the lateral condyle OCD shown on the right hand side of the radiograph on theright (brackets). There is also a small medial condyle cyst as well (arrow).


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cavity. Enlarging the slit-like articular surfacechanges the biomechanics of the cyst and no longerallows the entrapment of synovial fluid within thecystic cavity. Weight bearing then does not pres-surize the cyst, allowing the bone to remodel andheal, often reducing the size of the cyst until itremodels the bone to normal architecture. Thisprocess may take months to eliminate radiographicevidence of the cyst. The elimination of the articu-lar surface defect and decompression of the cyst,however, will normally restore soundness as soon asthe condyle remodels. The articular defect is onlyof consequence if the defect in the articular surfaceis sufficiently large to change the shape of the sur-face and create a biomechanical injury to the jointsurface or if the cyst has shed sufficient debris tosignificantly damage the adjacent articular surface.

Removal of the unsupported OCD over the cysticcavity to change the biomechanics within the cystdoes not require enucleation of the cystic cavity, andthis author often just removes the OCD and leavesthe contents of the cyst. Hypothetically, cell popu-lations within the cyst changed from predominantlybone-forming cells to bone-removing cells to formthe cyst, and therefore, removing the stimulus forthis change should revert the population to bone-forming cells within the cystic cavity, allowing thecyst to fill with bone more quickly than if the cyst istotally enucleated.

Injection of the cystic cavity with corticosteroids toreduce the inflammation has been described.63

This seems to be an effective means of eliminatinglameness, but this treatment does not change themechanics of the articular surface or materially al-ter the size of the cyst. The biomechanics of cystcreation remain, and in the author’s experience, re-occurrence of lameness can occur with resumption ofstrenuous exercise. Removal of the unsupportedarticular surface is recommended, if the cyst is caus-ing lameness.

In a growing horse, the articular surfaces, whichcontribute to growth until the horse is mature, willsometimes grow progressively from the margins and

close the articular communication. If this occurs,the cyst will disappear spontaneously. After a cystloses its communication with the articular surface,it will remodel and resolve. This is an indicationfor not treating cysts surgically unless they are en-larging or causing lameness.

The majority of distal metacarpal cysts that arefound when radiographing horses for other causesare innocuous, many resolving on their own, but ifthey are causing lameness, arthroscopic removal ofthe predisposing OCD lesion can be an effectivemeans of reversing the progression. The prognosisdepends on the size of the cyst, the amount of re-modeling of the condyle, and the condition of theinterior of the joint should the cyst be sheddingbiologic or mechanical debris into the articulation.Cysts seldom resolve after they begin to cause lame-ness in the fetlock joint, so lameness is an indicationfor treatment.

Proximal P-I Cysts

Proximal P-I cysts are rare and will occasionallyresult from an OCD, but they are more likely asequel to sagittal fractures of the first phalanx in theadult horse. If the sagittal fracture has not healed,then compression of the fracture by lag-screw fixa-tion is the best treatment to close the defect in thearticular surface. But, cysts seldom form until thefracture has partially healed, preventing compres-sion and closure of the surface defect.

The fracture-induced cysts follow the same pat-terns of development as the OCD-induced cyst, be-ing initiated by the traumatic slit in the articularsurface that is created by the sagittal fracture.Treatment, however, is less straightforward, be-cause the joint surface where they are formed can-not be accessed from the joint cavity, so an indirectapproach of drilling from the dorsal aspect of thebone is normally used. An attempt is then made todisrupt the articular cartilage slit from beneath thecartilage and enlarge the communication with thejoint to prevent pressurization and allow healing.The act of drilling enlarges the cystic cavity and

Fig. 24. This radiograph shows a distal McIII cyst. The intra-operative picture shows the articular surface over the cyst (brackets).


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along with opening of the joint surface, reduces thelikelihood of pressurization of the cyst on weightbearing, which will allow healing. If the cyst can beadequately exposed, the chances of resolution aregood.

Occasional proximal P-I cysts of the condyles ofthe articular surface will occur, but these cysts nor-mally are part of a process of severe degenerationand do not warrant treatment as a separate entity.If the degenerative process is advanced, they can bepart of a severely painful process. Treatment of thesevere degeneration sometimes requires arthrodesisto reestablish pain-free use of the limb.

Fractures of the First PhalanxSagittal fractures of the first phalanx are a commonaffliction of the Standardbred and Thoroughbredracehorses trained and raced on turf surfaces.64

Sagittal fractures acquire their name from the planeof fracture, which is parallel with the McIII sagittalgroove, splitting the first phalanx, usually in thesagittal groove. In most instances, the fracturestarts at the proximal articular surface of the firstphalanx, although occasionally, a fracture will beslightly parasagittal still in the sagittal plane.This fracture has all of the characteristics of a stressfracture, because it is seen in all degrees of propa-gation—in the sagittal plane but always starting atthe proximal articular surface (Fig. 25).65 Somevery short fractures only affect the proximal articu-lar surface where the fracture initiates. Fracturesof various lengths extend from proximal to distalinto the mid-P-I. The propagation of the fracture isdetermined by the amount of load subsequent tofracture initiation. The speed and accuracy of di-agnosis and the severity of the exercise period thatcreated the lameness determine how far the fracturewill propagate.

It is tempting to blame the anatomy and the“screwdriver” effect of the sagittal ridge of the can-

non in the sagittal groove of the first phalanx as thecause; however, this fracture rarely occurs in horsesthat work twisting and turning. It is most commonin horses that train on straight or gently curvingpaths. If the fracture happens early in the courseof an exercise period, then it is likely that the frac-ture will propagate further into P-I. Nearly allfractures initiate proximally and propagate distallyto the small medullary cavity in the distal one-halfof the first phalanx. At that point, in some horses,the fracture will exit abaxially, usually through thelateral cortex at the level of the small medullarycavity, creating a bipartite fracture that involvesonly the proximal articular surface. Alternately,the fracture may propagate distally through thesmall medullary cavity and become biarticular as itenters the pastern joint.

Short sagittal fractures can be difficult to diag-nose. With careful digital palpation of the nor-mally tender dorsal cortex of P-I and digitalradiography, one can make the diagnosis in mosthorses. In most instances, the lameness is signifi-cant, and the diagnosis is a differentiation of whichof the four bones of the fetlock joint has been injured.More severe fractures have localized swelling.

After the sagittal first phalanx fracture is con-firmed, the treatment is straightforward. No treat-ment compares with lag-screw fixation for speed ofhealing, quality of healing, and restoration of ath-letic ability.65–67 Therefore, lag-screw fixation offirst phalanx fractures is the treatment of choice.Reports of case series describe healing of these frac-tures using either stall rest or stall rest with exter-nal coaptation with casts or supporting bandages.64

These are treatment options, depending on theneeds of the horse. However, they are accompaniedby some risk of displacement, because the fractureoriginates in the sagittal groove of the first phalanxand can be easily displaced by pressure from the

Fig. 25. These three radiographs show a progression of severity of sagittal P-I fractures (arrows). The left fracture is incomplete,the center fracture exits the lateral cortex, and the right fracture is a biarticular fracture.


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sagittal ridge of the cannon bone should the horseplant its foot and twist. However, well-documentedsuccesses in a large percentage of cases have beenpublished using these non-surgical techniques.64

Over time, more and more horsemen and surgeonsfavor the internal fixation alternative because of itsspeed of healing and quality of recovery.

The surgical procedure is normally done with thehorse in lateral recumbency, although it could bedone in dorsal recumbency, if desired.67 The tradi-tional method of fixation is to insert screws in thetransverse plane starting just distal to the articularsurface. The author’s preference is to use a trian-gular screw configuration with two screws placedjust distal to the proximal articular surface—onecranially and one caudally (Fig. 26). The thirdscrew is inserted distal to the first two screws andproximal to the small medullary cavity of the firstphalanx. With the use of two screws just below thearticular surface, the restoration of soundness andthe amount of callus on the dorsal aspect of the firstphalanx is decreased, presumably indicating ahigher degree of stability.

The screws are inserted in lag fashion using stan-dard techniques. A cast is normally used for recov-ery from general anesthesia. The cast is onlynecessary for the initial post-operative period. Itcan be removed soon after recovery as per the sur-geon’s preference. It is unnecessary for the healingof the fracture, because the lag-screw fixation is verystable and capable of allowing the fracture to healwithout external coaptation. Normally, the frac-ture should be well bridged and beginning to re-

model by 60 days; at 90 days, resumption of normalactivity can occur. The prognosis for monoarticularsagittal fractures of the first phalanx is excellent,and restoration of athletic ability to the former levelis expected. Biarticular fractures are a bit moreproblematic, because the pastern joint is more likelyto become arthritic after this fracture than the fet-lock joint. The prognosis for athletic activity is stillgood if the surgical procedure stabilizes the fracturewell and the healing occurs without unduereaction.67

Displaced fractures are treated by open reductionand internal fixation, and as long as the fractureremains principally in the sagittal plane, the prog-nosis is excellent, if the fracture is minimally dis-placed. Significantly displaced fractures involvethe distal sesamoidean ligaments, which can causepersistent lameness.

The progression in severity becomes more difficultto resolve as the fracture becomes comminuted.68

The simplest comminuted fracture is a sagittal frac-ture that also fractures one or both of the palmareminences of P-I (Fig. 27).65

After this fracture occurs, permanent damage hasnormally been done to the horse’s athletic career.The degree of insult that is required to create thisfracture normally results in damage to the soft-tis-sue supporting structure of the palmar aspect of thefetlock joint, principally the distal sesamoidean lig-

Fig. 26. This radiograph illustrates the use of two screws im-mediately below the articular surface.

Fig. 27. This sagittal P-I fracture also has medial and lateralwing fractures of the proximal first phalanx.


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aments, and persistent lameness in spite of a goodhealing response by the bone is common in the au-thor’s experience. Therefore, after the fractureprogresses from a sagittal fracture to one with com-minution, the prognosis is decreased. The treat-ment approach is the same: repair of comminutedfractures requires fracture stabilization throughlag-screw fixation. However, in this instance, post-operative external coaptation is required and needsto be maintained until the fracture is bridging andstable.65

As the comminution becomes more extensive, thedifficulty of reconstruction increases, and the prog-nosis decreases. The presence of one cortex thatextends from the fetlock to the pastern joint mark-edly aids reconstruction of the bone and the progno-sis.68 After healing, these horses with thesefractures have an excellent prognosis for breedinganimals and in some instances, are useful for lessstrenuous activity, but generally, with comminu-tion, the fracture ends an athletic career.

The most severe fracture of the first phalanx is themultiply comminuted axially unstable fracture ofthe first phalanx.

These fractures have no intact cortex from proxi-mal to distal P-I. In the absence of that cortex toaid the reconstruction, some type of external weight-bearing support using a coaptation frame or a trans-fixation pin cast must be used.69 The author’spreference is the multiple pin cast (Fig. 28). Thecast transfers the weight from the metacarpus ormetatarsus through the cast to the ground until thefirst phalanx has healed sufficiently to allow weightbearing.70 The prognosis for healing of commi-nuted fractures is favorable, although it is accompa-nied by a higher incidence of laminitis in theopposing weight-bearing limb than would be ex-pected from other types of first phalanx fracturesand attempts at salvage have to take this into con-sideration.68 Treatment of the multiply commi-nuted P-I fracture is considered only for salvage andnot for return to athletic activity. However, if heal-ing occurs in an uncomplicated fashion, the horsecan be functional and live a normal, unrestricted lifeas a breeding animal after the healing is complete.68

Free Fragments in the Fetlock Joint

OCD lesions and occasionally, chip fractures can beshed to become free fragments within the fetlockjoint. When a free fragment occurs within a fetlockjoint, it normally moves about randomly untiltrapped in one of three locations. The most com-mon location for a free fragment is in the palmar orplantar pouch intermingled or encased in the syno-vial fronds of the proximal plantar or palmar pouchof the fetlock joint. Radiographically, the free frag-ment can be seen within the palmar/plantar pouchsoft tissue. This is an innocuous location for thefragment, because it does not interfere with the ar-ticulation of any of the four bones of the joint.

A second location where free fragments are com-monly found is in the small depression on the abax-ial aspect, medial or lateral, of the cannon bone,usually just cranial to the collateral ligament. Thearticular surface of the distal cannon bone extendsaround the margin of the joint into the medial andlateral condylar fossa to facilitate the highly mobilecollateral ligament in its path along the abaxialaspect of the bone. The fragment often becomeslodged in the condylar fossa. These are seen asradiographic free bodies adjacent to the edges of thedistal cannon bone.

The third location of free fragments is betweenand distal to the sesamoids in the small cul-de-sac ofthe fetlock joint just distal to and below the sagittalgroove of the first phalanx.

As long as the fragments stay in one of these threelocations, they are innocuous. Eventually, most ofthem become covered by fibro-cartilage and are non-

Fig. 28. This multiply comminuted P-I fracture is in a fiberglasscast and is supported by multiple pins through the metacarpusand the cast. Two lag screws were used to adapt the fetlock jointsurface.


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irritating to the surface of the bone. However, ifthe fragment dislodges and then passes through thearticulation, it can do damage to the articular carti-lage, and on passing through the interface betweenthe cannon bone and the first phalanx or the cannonbone and a sesamoid bone, it causes severe pain.A marked acute lameness, in some instances caus-ing the horse to carry the limb for a few stridesbefore reinitiating a normal gait and becomingsound again within a few strides, is characteristic ofa free fragment passing through an articulation.Based on the author’s experience, the acute stretchon the stabilizing soft tissues of the joint is severelypainful but resolves quickly if the fragment exits thejoint surface. A history of acute, severe lamenessthat only lasts a few strides is highly suggestive of afree fragment. It is possible for some free frag-ments to become trapped between the articular sur-faces, causing severe damage, but most progressthrough the articulation and end up in one of thecommon locations.

If the free fragment is causing lameness and/oreffusion, it is best removed arthroscopically. Freefragments found coincidentally that are not causinglameness in heavy-use horses are generally removedas well, because, in the author’s experience, the dis-lodging of a fragment into the articulation is notpredictable and may occur at any time. Arthro-scopic removal is normally a straightforward re-trieval in the palmar or plantar pouch, above orbelow the sesamoids. Dorsally, the retrieval isdone partially by arthroscopic palpation, viewingthe cannon bone margin and the abaxial aspect ofthe joint and palpating the depression where thefragment is lodged. After surgical removal, theprognosis is favorable unless the origin of the freefragment is causing lameness.

15. Diseases of the McIII/MtIII Sesamoid Articulation

Palmar/Plantar Distal Cannon Bone Injury

Inflammation of the Distal Cannon Bone

Inflammation of the distal cannon bone is one of themost common clinical problems seen in the Thor-oughbred racehorse. It is also seen in the Stan-dardbred racehorse and can be seen on occasion inhorses of other athletic disciplines such as showjumping and dressage.71 When wear and tear onthe bone accumulates because of high-level trainingstress, the microdamage stimulates the bone to re-spond.72–74 When bone must adapt to high-levelexercise by increasing its strength, it has one of twooptions. The bone can alter its structure or it canalter its shape to prevent the wear and tear damageof increasing levels of athletic activity.75

In most situations of high-strain loading, the boneuses both response possibilities to adapt to the newloads. It adds additional stronger bone and altersits shape to better neutralize the new and increasedloads being experienced. But, the distal aspect of

the cannon bone cannot alter its shape, because it ispart of the fetlock joint surface, which has a 270°radius of motion and an unalterable, cartilage-cov-ered joint surface. Therefore, the only possible ad-aptation that can occur in the bottom of the cannonbone is an alteration in the structural strength ofthe bone, because it cannot change shape. Thebone of the distal aspect of the metacarpus or meta-tarsus must become considerably stronger by becom-ing denser. Trabecular bone is nearly converted tocortical bone at the bottom of the metacarpus andmetatarsus. This adaptation takes time and sacri-fices the stress absorption capability of the bonewhen the cancellous bone is hypertrophied to thepoint that it is nearly cortical.76

Bruising of the bottom of the cannon bone resultsfrom accumulation of damage at a rate in excess ofthe bone’s ability for repair and is a relatively com-mon cause of pain. This is commonly termed mal-adaptive bone remodeling, but at this stage of thedisease, it is likely that the adaptation is normal butthe rate of stress accumulation exceeds the capacityof the bone to respond. A pathologic process is notyet present but the capacity of the normal boneresponse to manage the rate and degree of stressapplication is exceeded. Bone bruising accumu-lates and results in inflammation, pain, and lame-ness, similar to bruising at any site. If you examinethe palmar articular surface of most racing Thor-oughbreds grossly, some degree of this bruising ispresent grossly and histologically (Fig. 29).77 Thecycle of overload of the bone causing microdamagefollowed by over-repair to strengthen the bone is thecycle that is repeated over and over to train bone.78

If the over-repair gets behind the overloading, thebone begins to be damaged or bruised. As thebruising reaches a certain threshold of inflamma-tion, pain ensues.77

The distal cannon bone bruising is usually bilat-eral and often quadrilateral when the stress of train-ing exceeds the bone adaptation. The mostcommon presenting complaint is not lameness butrather decline in performance, weakness, and insome instances, even complaints of ataxia because ofthe gait alteration. Behavioral alterations are alsofrequent. Horses that formerly trained willinglyand then become reluctant to train commonly havebilateral or quadrilateral distal cannon bonebruising.

Predisposition to InjuryMuch has been made of conformation abnormalitiesleading to the higher incidence of certain injuries.79

Reports document an increased risk of fetlock jointinjury associated with certain conformations. Va-rus conformation of the forelimb has been shown toincrease the incidence of dorso-medial P-I chip frac-tures in the fetlock joint.79 But, for all but theextreme conformational abnormalities, the horse isamazingly adaptable to a wide range of conforma-tion variations in the fetlock joint.80,81


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Training methods are commonly accepted as hav-ing an influence on the incidence of injury inhorses.73,82–85 Some trainers have developedmethods that rarely result in serious injury and stillcreate horses that are able to compete effectively,but the opposite is also true.

There are two predispositions for an increasedrisk of lameness and injury that we have inadver-tently created in the highly trained equine athlete.These risks encourage damage to the palmar distalcannon bone because of their propensity to increasethe load and reduce the ability for repair of the distalcannon bone damage.78,86 The first is daily shortbursts of high-intensity exercise with prolonged pe-riods of stall rest. This system of training is neces-sitated by the high concentration of horses in areaswhere there is limited opportunity to remove themfrom the stall and by the tenuous shoe/foot structurethat causes horses to lose shoes if allowed free-choice exercise in solid footing.

In the ideal scenario, the horse is allowed freechoice exercise for much of the day, mimicking theevolutionary natural state. Naturally, horsesspend most of the day slowly walking and grazing.Because horses have no valves in the veins of thedistal limb, they are prone to limb edema secondaryto venous stasis if confined. They also have no sig-nificant muscle mass below the carpus and tarsus,

and therefore, they have little blood flow demand inthe lower part of the limb in most instances. Cir-culation in the lower limb is stimulated by the waya horse grazes. They eat a few mouthfuls, walk afew steps, then eat a few mouthfuls, and walk a fewsteps in a continuous pattern covering acres ofground in each day’s grazing. But when horses areconfined to a stall for the major part of the day, thehorse spends most of the day standing.87 This re-sults in passive edema or “stocking up” in the lowerpart of the limbs, which we have counteracted by theuse of stall bandages to keep pressure on the exte-rior of the limb and prevent the lymphatic edemathat results from circulatory stagnation.

But, these “stall bandages” do little to aid thecirculation of the bone, and hypothetically, they ac-tually increase the soft-tissue resistance to the cir-culatory exit of blood from the bone, which has aninterior-to-exterior circulatory pattern. When un-dergoing high-speed exercise training, bone needsactive motion to facilitate blood flow through thebone for the metabolic needs, which are increased bythe trauma and repair of the daily exercise trauma.

Bone circulation is a low-pressure system.35,36,88,89

Passive edema on the venous side of the circulationslows the return of blood to the circulation and in-creases the circulatory resistance, encouraging in-terosseous hypertension. External compression caneffectively reduce soft-tissue edema, but resistance toblood outflow facilitates intraosseous hypertension,causing inflammation and pain.35,36,88,89

In the author’s clinical experience, the currentmanagement of daily exercise impedes the horse’snatural osseous circulation needs and increaseschances for remodeling disease. The wear and tearof high-speed exercise concentrated in short periodsof time followed by confinement for most of the restof the day reduces the natural circulation that aidsrepair and creates the not surprising result of nu-merous bone remodeling diseases that we see clini-cally in our equine athletes.

There is no easy solution for current horse-exer-cise management because of space restrictions, andcreation of year-round racing and performance cal-endars allow this type of management to affect morehorses. When horses had forced periods of non-competition, alteration of training regimens and re-duction of exercise were the rule, which resulted inbetter remodeling activity for at least some periodeach year. This facilitated the healing and pre-vented the chronic wear-and-tear diseases that seemto be more frequent.

Our inability to maintain shoes on a fit racehorseduring periods of free-choice exercise also makes itdifficult to use paddock activity for many horses.However, even a period of walking exercise a secondtime during the day should be helpful to thecirculation.

The second predisposition to injury that we havecreated is traction devices on the forelimbs. Spe-cifically, toe grabs have been associated with the two

Fig. 29. This intra-operative photograph of the distal aspect ofthe metacarpus illustrates bone bruising (arrows) of the bottom ofboth condyles of distal McIII. The cartilage has been removedfrom the lateral condyle. Note that the articular cartilage isgrossly normal over the bruise.


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major catastrophic structural failures in the Thor-oughbred: disruption of the suspensory apparatusand condylar fracture.90,91 Experiments using in-strumented shoes to examine the effect of toe grabson the horse’s limb have shown that the accelera-tion/deceleration force is greatly increased by toegrabs.92,93 But, the increase in force is not in thedirection that one might first anticipate. Toe grabsare used for traction on the foot during the propul-sion phase of the horse’s stride, but the highestforces are generated in the horse’s limb during im-pact with the ground during deceleration when thetoe grab increases the braking effect.92,93 On softsurfaces, the toe has a toe-down progression on land-ing as the toe progresses inward and downward intothe soft surface, having the effect of raising theheel.94 The addition of the horse’s toe grab to thehorse’s toe increases the downward progression ofthe toe in a soft surface. Turning the toe down hasthe effect of raising the heel, lowering the fetlock,and pre-loading the suspensory apparatus beforethe application of weight.95,96 This change in theposition of the foot increases the stress or force thatthe suspensory apparatus experiences when thehorse loads the limb. This anatomic “pre-load” hasthe effect of increasing the load on the suspensoryapparatus and the condyles of the distal cannonbone during exercise.97

Because the forelimbs function biomechanicallyquite differently than the hindlimbs, the effect islikely different in the hindlimb. So, the correlationto injury in the biomechanical forces measured inthe forelimbs cannot be transposed to the hindlimbswith the same expected effect. But, the associationof traction devices and forelimb injuries encouragesmoderation or elimination of their use.

If the bruising of the distal cannon bone is bilat-eral or quadrilateral, the diagnosis can be challeng-ing, because a single limb does not appear to belame. The diagnosis is best made with diagnosticlocal anesthesia of the distal cannon bones to con-firm the site of pain. Nuclear scintigraphy is not aspecific indicator for this disease, because manyhorses have significant uptake in the distal meta-carpus and metatarsus that is not accompanied bysignificant pain.71,78,98,99 So, the only diagnosticcriterion of dependable significance is the disappear-ance of the lameness after local anesthesia of thedistal aspect of the metacarpus/metatarsus.

Fortunately, diagnostic local anesthesia can beaccomplished in a relatively specific fashion usingthe palmar metacarpal and metatarsal nerves.Local anesthesia of one of the limbs will result ineasily identifiable lameness, because the pain re-mains in the contra-lateral limb. Inflammation ofthe distal cannon bone (Fig. 30) will occur in eitherthe medial or lateral condyle in the forelimb, but it isalmost exclusively a lateral condyle disease in thehindlimb. The reason for this is unclear.

If bruising of the bottom of the cannon bone isdiagnosed early and the horse is given rest early

before anatomic changes occur, the prognosis forresolution is excellent. The rest from training mustbe in the form of paddock exercise, however, and notstall rest. Confinement to a stall contributes to thecreation of this problem and prevents the remodel-ing needed to heal the chronic bruising of the bone.Allowing the horse free-choice paddock exercise bestfacilitates the healing process. Free-choice exer-cise is the ideal treatment, because it best emulatesthe natural grazing stimulus of loading and unload-ing the bone continuously that facilitates osseouscirculation and remodeling. Vasoactive drugs toimprove the blood flow through the bone, which isassumed to be in a hypertensive state similar toinflammation in other bones, would also be a logicaltreatment and may help bone remodeling.

If training is continued in spite of the accumula-tion of damage, one of several pathologic conditionswill occur. Condylar fracture, palmar articularfracture, and palmar articular degeneration withalteration of the shape of the distal cannon bone areall possible sequelae. The prognosis is directly de-pendent on the degree of change in the bone archi-tecture as a result of the accumulated damage.

The most effective approach to this disease is di-agnosis before anatomic damage to the cannon boneand removal from training before anatomic derange-ment occurs. Retrospective analysis of horsestreated with a period of rest after a diagnosis of painlocated in the distal metacarpus or metatarsus hasbeen shown to be successful in allowing the bone torecover.100

Fig. 30. This flexed dorso-palmar radiograph of the distal McIIIshows bruising with demineralization (bracket) on the lateralcondyle.


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The process of accommodation of the articular sur-face of the distal cannon bone occurs in most horseswithout incident; however, bruising and inflamma-tion of the distal cannon bone as a part of the ac-commodation to high-level exercise is likely thesingle most common affliction that a high-speed ath-lete must overcome to reach its athletic potential.There are several major fetlock joint injuries thatare part of the disease complex initiated by damageto the palmar/plantar distal cannon bone articularsurface. The number of pathologic events that thechronic high-speed exercise loading can take in thedistal cannon bone presents somewhat of a dilemmain understanding the pathology.101 Why somehorses accommodate without problems and whysome horses sustain parasagittal fractures of thecondyles, whereas other horses simply accumulatethe load over time, resulting in collapse of the artic-ular surface of the distal cannon bone is not clear.Anatomy is certainly one of the considerations; con-dylar fractures predominate on the lateral condyles,and palmar articular degeneration predominates onthe medial condyle in the forelimb. In the author’sexperience, training regimens seem to be factors;many stables rarely experience this problem,whereas some have a high incidence.

Condylar Fracture

Condylar fractures are parasagittal fractures of thedistal articular condyles of the metacarpal andmetatarsal bones. They are one of the most fre-quent fractures in the racehorse.102–104 Condylarfractures are one of a complex of the distal cannonbone injuries that originate from the stress accumu-lation within the distal palmar/plantar articularcondyles of the cannon bone that accompanies high-speed exercise.105 When the progressive accumula-tion of the stress of exercise begins to exceed the rateof repair, structural damage ensues. The condylarfracture originates on the palmar/plantar aspect ofthe bone in the area where the sesamoid bone artic-ulates with the condyle.105 It is much more com-mon in the lateral condyle than in the medialcondyle for reasons that are not readily apparentanatomically, because the medial condyle is largerthan the lateral condyle and accepts more weight.106

Perhaps weight distribution plays a role in the cre-ation of the fracture.

It is generally accepted that accumulation ofstress and creation of microfractures are the initiat-ing causes of the condylar fracture.107 The micro-fracture creation in the palmar/plantar condylararea progresses until enough coalescence occurs thata macrofracture begins. The macrofracture beginsat the articular surface and progresses proximally ina sagittal plane. Condylar fractures are diagnosedin all degrees of propagation from very short frac-tures just being initiated at the articular surface tocomplete displaced fractures.104 This spectrum offractures following generally the same plane but in

varying degrees of progression is typical of stress-fracture initiation and propagation.

Lateral fractures most often propagate abaxiallyfrom the site of initiation on the axial two-thirds ofthe lateral condyle and exit the cortex 7–8 cm prox-imal (Fig. 31) to the fetlock joint, but they can occurmore axial or abaxial and propagate axially or ab-axially.104 Medial fractures more often propagateaxially and can progress proximally as far as theproximal metaphysis of the bone. If the fracturespropagate until they exit during exercise, they willdisplace and set off a chain of events that destabi-lizes the fetlock joint, which may result in disartic-ulation. Fortunately, most but not all condylarfractures show signs of lameness before completionand are diagnosed before the fetlock anatomy isdestroyed.

Retrospective analysis of a large group of condylarfractures has shown that the configuration into thearticular surface plays a role in the eventual prog-nosis.104 The presence of articular comminution onthe palmar/plantar condyle articular surface re-duces the prognosis for a return to racing after sur-gical treatment of this injury. This comminutionseems to be a hybrid of the palmar distal cannonbone semilunar fracture and the condylar fracture.The wedge-shaped articular comminution often oc-curs in areas of inflammation in the distal aspect ofthe cannon bone, at the same location that the con-dylar fracture occurs. The fracture can start as apalmar articular fracture, eventually progressing toa condylar fracture.

Fig. 31. This radiograph shows a complete displaced lateralMcIII condylar fracture.


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Diagnosis in recent years has been greatly aidedby a better understanding of the pathophysiologyand anatomic configuration of this injury. This un-derstanding has been facilitated by the newer radio-graphic and scintigraphic technology that has betterelucidated the pathology of this injury.

If the condylar fracture is discovered as a finefissure fracture of only the palmar condyles, thenthe injury is stable, and no surgical treatment isneeded. If the injury progresses proximally andcertainly, if it can be seen on the flexed dorsal pal-mar as well as standing dorsal palmar radiographs,the fracture benefits from surgical treatment by in-ternal fixation in both the speed of healing and thequality of recovery. Condylar fractures that arenon-displaced have historically been treated by thenon-surgical means of confinement and exercise re-striction. But, experience has taught veterinariansand horsemen that the most rapid, most functionaloutcome occurs with compression and stabilizationof the fracture through open reduction and internalfixation with lag screws. The prognosis is directlyrelated to the severity of the injury.103,108

Displacement of the fracture adds to the severityof the injury and decreases the prognosis, as doesarticular comminution. Articular comminutiondoes not preclude the successful repair if the artic-ular comminution can be reduced and reconstructedwith the reconstruction of the primary fracture.But, if a defect in the articular surface persists, theprobability of a successful repair is greatly reduced.The goal of most condylar fracture repairs is resto-ration of athletic activity, which is achievable withsuccessful internal fixation and anatomic recon-struction. Any residual articular defects or malre-duction of the condylar fracture greatly reduces oreliminates the chance of racing.108 The margin forerror is quite low in this heavily loaded joint surface.

The surgical repair is normally approached fromthe ipsilateral aspect of the injury, and non-dis-placed fractures can be stabilized without articularvisualization for reduction.108 Displaced fractures,however, should be visualized arthroscopically toassure anatomic reduction has been achieved. It isimpossible to assure this with only radiographic ex-amination of the injury intra-operatively, and there-fore, arthroscopic or open visualization of thereduction of the fracture is indispensable to the suc-cessful repair in displaced fractures (Fig. 32).

After the joint has been anatomically reduced andconfirmed visually, the fixation is technically similarin non-displaced and displaced fractures with theplacement of lag screws across the fracture. Twoscrews are most commonly used. The distal lag-screw location is most important. It should ideallybe concentrically located in the condyle of the distalcannon bone to provide compression on the entirearticular surface (Fig. 33).

Location of the screws is more difficult than onemight anticipate, especially when swelling of theinjury distorts the anatomy. Some surgeons repairthese fractures standing; because the location of thescrews in the ideal position is important and a fewmillimeters can make the difference between suc-cess and failure, the method that assures the bestpossible repair in the situation should be used.

Lateral condylar fractures and medial condylarfractures that do not displace or spiral proximallyrequire no external coaptation for recovery from an-esthesia if the internal fixation is acceptably done.Condylar fractures that spiral into the diaphysis ofthe bone and in some instances, propagate proxi-

Fig. 32. This arthroscopic picture shows the articular surface ofthe distal cannon bone after arthroscopic visualization and reduc-tion of a displaced condylar fracture (arrow).

Fig. 33. This radiograph shows the proper location of lag screwsfor stabilization of a condylar fracture.


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mally as far as the proximal metaphysis have in-creased risk for failure both in recovery and in thepost-operative period. Horses under the author’scare have displaced spiraling condylar fractures aslate as 6 wk post-injury. Publications have de-scribed the placement of multiple screws in a stand-ing horse to obviate the need for recovery fromgeneral anesthesia. But, in a situation where thedifference between success and failure with condylarfractures can be a matter of millimeters of variancefor ideal screw placement, careful anatomic reduc-tion and accurate screw placement in the condyles iscritical, and the addition of a neutralization plate tothe diaphysis of the bone to protect the bone duringthe healing period is preferred (Fig. 34).109

The reasons for using this technique are a morerapid return to soundness, reduced risk of displace-ment associated with the spiraling diaphyseal frac-ture both in recovery and during the post-operativeconvalescent period, and rapid, safe dismissal fromhospital care. In the author’s experience, horseswith spiraling diaphyseal fractures stabilized byscrews alone remained lame for weeks, but horseswith neutralization plates applied were sound im-

mediately post-surgery. The plate is placed intra-operatively, and then, after fracture healing hasoccurred, the plate is removed, often with the horsestanding, before reinitiating training. Horses oflesser use than racing tolerate a plate on the diaph-ysis of the metacarpus, but in an experimental studyperformed by the author, six of six horses becamelame as they approached race speeds with a plate intheir metacarpus. Therefore, for horses perform-ing high-speed exercise, such as racing, the plate onthe diaphysis of the cannon bone must be removed.

After repair, the normal aftercare requires �3 mo.The prognosis has been well documented, and onecan anticipate successful recovery with condylarfractures in most instances, including articular com-minution, if the fracture is anatomically reducedand stabilized.

Palmar semilunar fractures occur in some horsessubsequent to distal cannon bone inflammationwithout a sagittal condylar fracture and before thedegeneration of the condyles (Fig. 35). If thesefractures are small and especially if they are taller(proximal to distal) than they are wide (medial tolateral), training in their presence will result in acondylar fracture. If the semilunar fracture iswider than it is tall, then lameness sufficient toprevent exercise usually ensues before a condylarfracture is created. Palmar semilunar fracturescan heal if they do not separate from the parentbone. If they separate from the parent bone, theyusually progress to degeneration with reabsorptionand degeneration of the articular surface. The

Fig. 34. This spiraling medial condylar fracture (arrow) waspropagated through the mid-diaphysis and was stabilized usingtwo lag screws across the metaphysis and a dorso-lateral neutral-ization plate.

Fig. 35. This radiograph shows biaxial semilunar fractures ofthe distal cannon bone (brackets).


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semilunar fracture that separates from its parentbone has no blood supply. It is totally intra-artic-ular. If interface with the parent bone is unstable,there is no chance for healing, and joint function islost.

Therefore, a period of stall rest is normally thetreatment for this fracture. It cannot be stabilizedsurgically, and exercise encourages instability.If the fracture separates from the parent bone ordepresses into the parent bone during the healingprocess, the prognosis is poor. If healing occurswithout alteration of the shape of the articular sur-face, the horse has a good chance of returning toathletic activity.

Palmar Articular Degeneration of the Distal Cannon Bone

The medial condyle of the forelimb is the most likelyto accumulate structural damage to the subchondralbone and undergo alteration of the shape of the bonewith collapse and flattening of the articular sur-face.110,111 It is unknown why a condylar fractureis more likely on the lateral condyle and the palmardegeneration is more common medially, but there isan obvious size difference in the two condyles.This may play a role, but either condition can occuron either condyle.

The term maladaptive applies in this conditionbecause of the progressive alteration of bone anat-omy in response to exercise stress rather than theaccommodation to exercise that is needed. Perhapsthis is just application of stress in excess of theability of the bone to respond.111 The degenerativeremodeling process results in irregular areas of boneabsorption and production, and when combined withweight-bearing stress, it causes the collapse of thenormal architecture of the condyle.105,110,111

The change in shape of the cannon bone alters thecongruence of the articulation with the face of thesesamoid, increasing the joint surface damage andeventually, causing palmar degeneration of the ar-ticular surface. Palmar articular degeneration caninitiate fractures of the distal cannon bone, but inmost instances, a condylar fracture does not occur inthe area of palmar articular degeneration. Sub-chondral bone collapse is more common than a con-dylar fracture.

This collapse of the joint surface because of thedamage to the supporting subchondral bone is ac-companied by damage to the cartilage.110 If train-ing continues in the face of this alteration and loss ofcongruence with the face of the sesamoid, a fractureof the base of the sesamoid is the common sequelae.

Palmar condyle degeneration may appear radio-graphically as simple flattening, but after the alter-ation in shape of cannon bone begins to occur,degeneration of the articular surface always accom-panies it (Fig. 36). The degree of damage to thepalmar articular surface determines the prognosis.One must be careful not to misdiagnose palmar con-dyle flattening as the radius of curvature of thearticulation of the distal cannon bone with the first

phalanx is considerably different than the radius ofcurvature of the sesamoid bone articulation andgives the appearance of palmar condyle flattening ifone is not aware of these different articulations.This leads to the misdiagnosis of palmar condyleflattening in the yearling, which never occurs. Pal-mar flattening is an acquired disease that occursduring training and usually after a significantamount of race participation, because it takesmonths of continuous loading to create the responsein the distal cannon bone.

Palmar articular surface degeneration and loss ofarticular surface on the palmar or plantar aspect ofthe distal cannon bone with flattening of the bone isa permanent change and virtually always results inchronic lameness. Occasionally, repair will occursufficiently to allow return to exercise at a lowerexercise level, but the damaged articular surfacerarely allows the horse to maintain its form afterradiographic flattening of the palmar distal cannonbone begins. Some horses are surprisingly tolerantof even significant degrees of palmar distal cannonbone ulceration for a time, and they are able tocontinue racing in a diminished capacity in spite ofthe fact that the articular surface has been breachedwith a loss of articular cartilage. However, at somepoint, the injury becomes intolerable in all horses,no matter what the treatment.

The career-ending clinical development is fre-quently a fracture of the base of the sesamoid bonethat results from the uneven biomechanical loadingof the sesamoid bone subsequent to the flattening ofthe articular surface of the distal cannon bone.Treatment of this type of base sesamoid fracture isunrewarding, because the treatment of the sesamoidfracture is simply treatment of the result and notthe cause of the fracture. The primary disease offlattening of the distal cannon bone persists. Thereis no surgical treatment for palmar distal cannon

Fig. 36. This radiograph shows flattening of the palmar distalaspect of McIII (arrowheads).


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bone degeneration, because debridement of the pa-thology on the bottom of the cannon bone simplyadds to the loss of articular surface and does notnegate the ulceration that accompanies the flatten-ing. This is a career-ending injury and can lead topainful degeneration of the fetlock joint, which mayrequire joint fusion.

SesamoiditisSesamoiditis by definition is inflammation of thesesamoid bone. More accurately, it is an inflamma-tion of the insertion of the suspensory ligament intothe proximal abaxial aspect of the sesamoid bonewhere the ligament is anchored into the bone.Sesamoiditis can and does occur in any of the eightsesamoid bones of the horse. Past confusion as tothe definition of sesamoiditis was partly resolved bya publication that separated the different radio-graphic characteristics including enlarged and in-creased numbers of vascular canals, proliferation onthe abaxial aspect of the sesamoid bone, and lucencyon the abaxial border of the sesamoid and docu-mented their effects on racing performance.39,112

In this study of the radiographic appearance of ses-amoiditis, vascular canals that were increased innumber but regular in nature with parallel borders�2 mm in diameter did not affect the horse’s perfor-mance (Fig. 37). As the vascular canals becamealtered in size with the canal borders becomingwider radiographically and usually adopting a some-what barrel-shaped appearance, the horses’ perfor-mances declined both in number and quality of racesas the number of canals increased. In anotherstudy where a different definition of vascular canalenlargement was used, no difference in performancewas shown.41 However, the incidence in this groupwas very high (79%) and may have clouded theresults.113

In my experience a decline in performance with ses-amoiditis occurs in horses with all uses.114 Horsesplace a significant load on the suspensory apparatus innearly all activities. Because the fetlock is a totallypassive joint with no option to reduce the load andprotect the joint voluntarily, sesamoiditis affectshorses used in most types of performance.

In one study, proliferation and lucency had littleeffect on athletic performance in racing Thorough-breds.39 It is probable that lucency in the area ofthe suspensory ligament attachment is important inthe acute stages of the inflammation. Becausethese studies were done on yearlings by the timethey began their athletic careers, it is probable thatthe lucencies seen may have healed. In anotherreport, osteophytes on the abaxial aspect of the ses-amoid bones in hind fetlocks were associated withdecreased performance.41

Marked irregularities of the suspensory insertionand significant demineralization in the attachmentsare certainly suspicious for disease of the insertionof the suspensory ligament into the sesamoid bone,but in the absence of enlarged vascular canals, theyare not predictive of decreased performance in year-lings. The enlarged vascular canals, however, wereproven to be a good indicator of decreased perfor-mance.39 It is likely that, similar to the distal ses-amoid (navicular bone), these enlargements in thevascular canal are markers for previous inflamma-tion in the bone.115,116 Unlike the navicular bonewhere they are not predictive of performance, thedamage seems to be irresolvable after the suspen-sory ligament insertion into the proximal sesamoidbone is damaged. The horse cannot recreate theexact structure of the natural insertion of the sus-pensory ligament into the sesamoid bone. There-fore, although healing may occur and theattachment of the suspensory ligament to the sesa-moid bone may be reconstituted with scar tissue, itis improbable than any type of scar tissue will beable to function in a fashion similar to the undam-aged suspensory ligament attachment to the sesam-oid bone. When the level of work is sufficientlydemanding, the fibrous tissue reconstitution of theligamentous insertion will fail. Therefore, thehigher the desired level of performance expected ofthe rehabilitated horse with sesamoiditis is, theworse the prognosis.

There is no surgical or medical therapeutic planthat can alter or improve the horse’s reconstitutionof the suspensory ligament anchorage into the ses-amoid bone after it has been lost. So, after thesuspensory ligament attachment is damaged beyonda certain point, it is permanently disabling, and thedegree of problem that it causes the horse is directlyrelated to the amount of sesamoid interface attach-ment damaged.

The prognosis is difficult to alter, because no treat-ment can reattach the suspensory ligament. How-ever, if active sesamoiditis is underway and theenlargement of vascular canals is ongoing and at-

Fig. 37. This radiograph shows sesamoiditis with three en-larged vascular canals (arrowheads).


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tended by lucency in the abaxial border of the sesam-oid bone at the suspensory insertion, attempts toreossify the sesamoid bone by reducing the inflamma-tion can help to mitigate the ongoing damage ofsuspensory ligament avulsion. When active sesam-oiditis is underway, damage to the suspensory liga-ment insertion creates inflammation. Inflammationin the bone causes bone reabsorption, further weaken-ing the suspensory ligament insertion, which predis-poses to further damage and stimulates furtherinflammation in a cyclic progressive manner. There-fore, removal from exercise stress and treatment of theinflammation within the bone is indicated.

Because hypertension within the bone is associ-ated with inflammation, it is likely that the samesituation occurs at the injured proximal sesamoidbone.35,36 Medications that aid blood flow throughthe bone without hypertension are hypotheticallyindicated. Aspirin or pentoxyfylline to alter theplatelet adhesive characteristics and capillary bloodflow as well as vasoactive drugs such as isoxsuprinemake therapeutic sense. This is the author’s rec-ommended treatment of choice, and although theresponse to this therapy is slow and not dramatic,these compounds seem to be the most effective of allof the treatments that have any effect on the sesa-moid bone and sesamoiditis.

Distal Sesamoidean Ligament Desmitis

There are four distal sesamoidean ligaments, theshort, cruciate, middle or oblique, and superficial orstraight, that attach to the distal aspect of the ses-amoid bones. Sometimes, publications inaccu-rately call these X, Y, Z ligaments. The short andcruciate sesamoidean ligaments are relativelysmall, and desmitis of those ligaments is rarely rec-ognized as a clinical entity. They play a role in thecreation of palmar/plantar first phalanx chip frac-tures, but primary desmitis is not discernable.The likely reason for this is that these ligaments areso small relative to the middle and superficial distalsesamoidean ligaments that they are of little conse-quence in the strength of the attachment of thesesamoid bone on the palmar/plantar aspect of thefirst and second phalanx in the loaded fetlock joint.

Middle distal (oblique) sesamoidean ligamentdesmitis causes significant lameness. The middledistal sesamoidean ligament’s origin occupies themajority of the base of the sesamoid; the distal in-sertion covers a large portion of the palmar/plantaraspect of P-I in a V-shape attachment extendingfrom just distal to the fetlock joint to just proximal tothe pastern joint. The middle distal sesamoideanligament is by far the largest of the distal sesam-oidean ligaments in its origin and insertion, andbecause of its size, it plays the largest role in thesupport of the fetlock joint below the sesamoidbones.117 Middle distal sesamoidean ligament in-juries are difficult to resolve for high-speed athleticactivities at any location other than at the insertionon the palmar or plantar aspect of the first phalanx.

If the middle distal sesamoidean ligament is in-flamed, thickening can sometimes be identified dis-tal to the sesamoid bones abaxial to the flexortendons, but most horses have no outward clinicalfindings, and the site of pain is identified with diag-nostic local anesthesia.118 Middle distal sesam-oidean ligament inflammation at its insertion on thepalmar or plantar aspect of the first phalanx is acommon finding in horses that perform twisting andturning athletic events. Fortunately, the insertionof the middle distal sesamoidean ligament on thefirst phalanx has considerable redundancy, and theinsertion enjoys a biomechanical advantage in itsoblique insertion into the bone, so structurally im-portant injuries of the distal insertion are seldomencountered. Complete disruption rarely, if ever,occurs at the first phalanx insertion, and in mostcases, desmitis of the distal insertion is only recog-nized after radiographic appearance of insertionproliferation shows that the insertion has been dam-aged or with sophisticated diagnostic techniques.118

Inflammation of the middle portion of the middledistal sesamoidean ligament is a major injury.The middle distal sesamoidean ligament is difficultto image because of the oblique nature of the liga-ment fibers. Therefore, the ligament must sustaina significant amount of damage before the ultra-sound examination can dependably detect the in-jury. The best diagnostic tool to determine thedegree of damage is MRI. The MRI is dependablyable to detect and determine the severity of middledistal sesamoidean ligament desmitis.118

Injuries of the middle distal sesamoidean liga-ment origin from the base of the sesamoid bones arevery problematic for high-speed activity. Unlikethe large oblique insertion into the first phalanx,which is biomechanically advantageous, the originof the middle distal sesamoidean ligament into thebase of the sesamoid proximally is perpendicular tothe base of the sesamoid bone and therefore, repairof that insertion is very difficult. It carries a de-creased prognosis similar to the suspensory branchinsertion into the abaxial aspect of the sesamoidbone, because it requires reconstruction of a nearlynon-reconstructable origin on injured bone.

After desmitis occurs to the degree that it showsclinical signs for both mid-ligament and proximalligament injuries to the middle distal sesamoideanligament, the horse is often permanently injured.Therefore, rest and rehabilitation is imperative, butearly diagnosis is the most important, althoughmost difficult, component of treatment. This liga-ment heals slowly and relatively poorly in mosthorses. Treatment through medical or surgicalmeans can resolve some injuries, especiallythe more distal injuries in performance horses.118

Racehorses with this injury are a much more diffi-cult problem, partially because they tend to be in-jured near the origin on the sesamoid bone.

Biologic therapy, such as stem-cell augmentation,theoretically has the best chance to optimize repair


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but has yet to show efficacy, and in the author’sexperience, it has not been very helpful. We haveyet to master the ability to insert these cells andaffect any significant repair. The use of these tech-niques for biologic repair has yet to be dependablysuccessful.119 The prognosis for an injury to thebody or proximal insertion of the middle distal sesa-moidean ligament is unfavorable.

Injury of the middle distal sesamoidean ligamentorigin at the base of the sesamoid bone is relativelycommon in the foal, and the small fragment avul-sions from the base of the sesamoid that are foundradiographically in young horses are markers of in-jury for this ligament (Fig. 38). These fragmentsare an indicator of a predisposition to further dam-age as high-speed exercise levels are reached.120

Removal has been recommended, but removal of thefragments removes the result of the injury and doesnot negate the primary problem of loss of distalsesamoidean ligament attachment; it may, in fact,add to that problem because of the difficulty of ac-cessing this area without damaging additional fi-bers.121 A few horses can overcome the presence ofan injury to this area, but most with fragments fromthe middle of the base of the sesamoid become lamebefore they reach strenuous levels of exercise. Thelameness is not the result of the osseous fragmentsbut rather is caused by the loss of the fibers of thedistal sesamoidean ligament that attach to the baseof the sesamoid. The remaining fibers usuallyprove insufficient for high-level exercise without in-jury and lameness.

Injury to the superficial (straight) distal sesam-oidean ligament will occasionally occur on the distal

abaxial aspect of the sesamoids on the abaxial distalborder of the sesamoid, but the majority of thosefibers insert into the more flexible base of the in-tersesamoidean ligament scutum between the sesa-moid bones. The superficial distal sesamoideanligaments tolerate insult relatively well at theirproximal origin compared with the middle distalsesamoidean ligament and are rarely injured clini-cally. The proximal attachments often do createosteophytes when they are injured in the juvenileanimal, but they rarely cause clinical lameness.The osteophytes are seen on the palmar/plantaro-lateral or medial margin of the sesamoid bone onradiographs.

Desmitis of the body of the superficial distal sesa-moidean ligament is also rare, and injury to thesuperficial distal sesamoidean ligament insertion atthe attachment to the second phalanx scutum is themost commonly identified injury. The prognosishas a direct correlation with the quantity of fibersinjured at the distal sesamoidean ligament inser-tion.122 But, if the injury has not detached a largeportion of the bone at its insertion, they are mostoften found as an incidental finding on radiographsand rarely, as part of clinical lameness. When in-jury is diagnosed, it is usually a result of its effect onthe pastern joint and not because of ligamentouspain.

The four distal sesamoidean ligaments have dis-tinct biomechanical injury predispositions of theirown related to their size and importance. The in-jury to the distal sesamoidean ligaments that ismost devastating is a complete avulsion of all fourligaments from the base of both sesamoids that oc-curs during high-speed activity in the racehorse.It often occurs with no warning, and because it is adisabling injury to the suspensory apparatus of thefetlock joint and cannot heal, it must be dealt withby circumventing the need for the suspensory appa-ratus. This is done with a fetlock arthrodesis.

Intersesamoidean Ligament Desmitis

The largest ligament in the fetlock joint is the in-tersesamoidean ligament. It occupies the entire in-terface between the two sesamoid bones and formsthe back of the sagittal groove where the sagittalridge of the cannon bone interfaces with the palmar/plantar support of the suspensory apparatus. Theintersesamoidean ligament is flexible in that it willallow the sesamoid bones to move independently ontheir respective condyles of the distal cannon bone,but the intersesamoidean ligament is strong enoughthat the sesamoid bones cannot move abaxially inrelation to each other. This ligament carries a highload. As the maximum weight is applied to thefetlock joint, the sesamoid bones translocate distallyon the bottom of the cannon bone; the sagittal ridgeof the cannon bone drives between the sesamoidbones while the suspensory ligament, which bifur-cates into the two branches, pulls abaxially on thesesamoid bones. The resistance to separation be-

Fig. 38. This radiograph shows an avulsion fracture of a portionof the middle distal sesamoidean ligament origin from the base ofthe sesamoid bone.


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tween the sesamoid bones requires a large ligamentto stabilize the sesamoid bones in the face of virtu-ally the entire weight of the horse, which is placedon the lead limb at high speeds.

When the intersesamoidean ligament or its at-tachment to the sesamoid bone is injured, it is oftenextremely painful for the horse. The degree of dis-comfort exceeds most injuries to the fetlock joint,because there is no opportunity for the horse toguard the ligament against loading. A very smalldisruption, if it does not structurally weaken thebone/ligament attachment, is tolerated,123 but insignificant intersesamoidean ligament desmitis orinjury, the horse will refuse to use the limb becauseof the pain.

Fortunately, injuries to the intersesamoidean lig-ament are relatively rare. Intersesamoideanligament desmitis, in many instances, is initiated byan infection but can be initiated by trauma.123

Unfortunately, there is no definitive treatment, andthe inflammation of the ligamentous insertion istreated similarly to sesamoiditis by attempting toreduce the inflammation and allow the damagedbone to strengthen the intersesamoidean ligamentattachment to the parent sesamoid bone. If this issuccessful, then restoration of function can occur,but the total resolution of inflammation and pain isdifficult and is the exception rather than the rule.Debridement of infection in the bones or ligament ishelpful but would seem to hold little benefit fortraumatic causes.

Palmar/Plantar Joint Capsule Avulsion

Palmar/plantar joint capsule avulsion from its pal-mar/plantar insertion on the distal cannon bone isseen in two instances. It is seen in the foal whentrauma, presumably torsion, pulls the fibers of thefetlock joint capsule from the growing bone. Theinjury is rarely diagnosed at occurrence, but it isnoticed when the bone and joint capsule respondwith a marked proliferative response that reat-taches the joint capsule to the palmar/plantar can-non bone. Lameness is rarely associated with theinjury. Rather, the appearance of the large re-sponse, the size of an adult human finger, attachedto the palmar/plantar abaxial distal cannon bone isdetected. After the joint capsule has reconnected tothe cannon bone, the large proliferation graduallyremodels and never persists into adulthood. Theradiographic change can be quite alarming in ap-pearance and persist for some time in the foal.

In the adult athlete, an injury to the joint capsuleinsertion onto the palmar/plantar of the cannonbone is often associated with an injury to the in-tersesamoidean ligament. The injury to the jointcapsule is rarely of long-term concern, but thedesmitis of the intersesamoidean ligament cancause lameness and affect performance. The injuryto the joint capsule can cause considerable fibrosis,but it rarely causes long-term lameness.

Palmar/Plantar P-I Chip Fractures

Palmar/plantar P-I chip fractures occur from P-Ieither in the plantar aspect of the hind fetlock,which is more common, or in the palmar aspect ofthe front fetlock.124–127 The palmar/plantar P-Ichip fracture is an avulsion fracture from P-I at theinsertion of the distal sesamoidean ligaments intothe first phalanx. The more axial fragments arepulled free by the cruciate distal sesamoidean liga-ment. They are more common than abaxial frag-ments and are normally within the fetlock jointunder the sesamoid bone. Most abaxial fragmentsoccur at the attachment of the short distal sesam-oidean ligaments and at the attachment of the pal-mar/plantar bundle of the collateral ligament on thefirst phalanx. Injuries to the short distal sesam-oidean ligament insertions on P-I create fracturesfrom the palmar/plantar abaxial aspect of P-I imme-diately distal to the abaxial aspect of the sesamoidand are similar in pathology to avulsion of the cru-ciate distal sesamoidean ligaments.

The fragments are always larger than they appearradiographically in the immature horse and occurwhen a fragment of growing bone is pulled free fromthe parent bone by the distal sesamoidean ligamentattachment to P-I. The fragment normally contin-ues to enlarge as the horse grows until maturity.The origin site heals simultaneously, often fillingwith bone. This leaves an enlarged fragment and adiminished fracture cavity. The result is a mobilepiece of bone between the sesamoid bone and thefirst phalanx that often articulates with the distalcannon bone during exercise. These avulsion frac-tures from palmar/plantar P-I are sometimes erro-neously called an OCD.42

The effect on the joint results from the fragmentprotruding into the joint. This may result in abra-sion/articulation with any of the three bones thatinterface with the fragment. The degree of pathol-ogy caused by this fracture fragment is directly re-lated to size. Small fragments can exist under thesesamoid bone without interfering with sesamoidbone, palmar/plantar first phalanx, or cannon bone,and after covered by fibro-cartilage and isolatedfrom the joint, they are innocuous. However, aftera fragment reaches a critical size large enough tointeract physically with the base of the sesamoid,the palmar/plantar aspect of the first phalanx, oroccasionally, the distal cannon bone during high-speed exercise. Rarely do they cause overt lame-ness, although this is sometimes possible. Inhorses that perform at the gallop, most often thecomplaint is that the horse is uncomfortable andprefers the opposite lead during exercise. The se-verity of the irritation is most apparent in the Stan-dardbred, where the complaint is frequently heardthat the horse will not stay in the proper gait.

If the fragment causes inflammation in the fetlockjoint or if it seems likely to be a problem with in-creased exercise, arthroscopic removal is a simple


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and very effective treatment. The arthroscope isused to visualize the fragment proximally, and thefragment is isolated and removed from the palmar/plantar aspect of the first phalanx.128,129 Surgicalremoval is often accompanied by the identification oferosions and softening on the palmar/plantar aspectof P1 or the base of the sesamoid bone where thefragment is interfering with the adjacent bone.These areas of interface result in debris sheddingand also can be irritating, because they begin toaffect adjacent ligamentous attachments, creatinglameness.

After surgical removal, the joint will be normal.The short and cruciate distal sesamoidean liga-ments are not large contributors to weight bearingby the suspensory apparatus and have been disabledby the detachment of the fragment from the firstphalanx anyway. Therefore, no significant weak-ening or damage to the fetlock support occurs withan injury to these ligaments. Removal eliminatesthe irritating fragment from the joint with little orno residual effect.127

The palmar/plantar bundle of the collateral liga-ment of the fetlock joint can create avulsion frac-tures of the abaxial aspect of the palmar/plantar P-I(Fig. 39). These fractures involve the wing of thepalmar/plantar P-I and are taller than they are widein the juvenile animal (Fig. 39). In the adult, theyare sometimes wider than they are tall. When theyoccur in the yearling, they are nearly always extra-

articular, but in the adult, they normally invade thejoint.

In the yearling, the fragments form delayed fi-brous unions that eventually mature to a bone unionwith time. The collateral ligament avulsion frac-ture that occurs in the immature animal rarelycauses lameness after the acute occurrence, unlessthere is a concurrent intra-articular fragment cre-ated by the distal sesamoidean ligament at the timeof the wing fracture creation. The intra-articularfragment may need to be removed, but theextra-articular wing fractures, although they areprominent radiographically, rarely cause lameness.With time, the fibrous delayed union, which occursin the yearling or 2-yr-old horse, matures to a boneunion. The fibrous union is perfectly functionaland normally requires no treatment.

Wing fracture of P-I in the adult, however, nor-mally involves the fetlock joint and causes lameness(Fig. 40). The smaller fractures that are widerthan they are tall are difficult to repair, and surgicalremoval is often the only option. The prognosis isaffected by the amount of joint surface involved, butthis is not a critical area for the function of thefetlock joint; removal of all but the very largest offragments carries a favorable prognosis.

The larger fractures that are taller than they arewide and significantly invade the fetlock joint arebest treated with lag-screw fixation to stabilize andcompress the fracture, restoring the fetlock jointarticular surface and preserving the collateral liga-ment attachment. With appropriate internal fixa-tion and healing, the prognosis is favorable forathletic use.65

Fig. 39. This radiograph shows the presence of both a plantarP-I chip fracture that is intra-articular (arrowheads) and a plan-tar abaxial P-I avulsion fracture that is extra-articular (arrow).

Fig. 40. This radiograph shows a plantar P-I fracture caused bya plantar bundle collateral ligament avulsion in an adult (arrow).


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Collateral Ligament Rupture/Luxation of the Fetlock JointCollateral ligament disruption with an open woundinto the joint is a topic for wound management.However, closed collateral ligament rupture is occa-sionally encountered. The fetlock joint does not re-quire collateral ligaments in the stance phase of thestride. The sagittal ridge, sagittal groove, andsesamoids make the joint stable when it is underload, and although lameness is present, the limb isstable.130,131 The collateral ligaments maintainthe normal anatomy when weight is off the limb.Closed rupture can be accompanied by rupture ofthe joint capsule as well. In mildly unstable limbs,only restriction of exercise is necessary. In mosttraumatic ruptures, cast immobilization will aid fi-brosis to adequately replace the ligament. Cast im-mobilization for �5–6 wk, depending on the horse’sprogress, is normally sufficient. It is preferential touse a cylinder cast to allow motion of the distalphalangeal joints, because this reduces the tendonlaxity that is created by enclosing the foot. Theprognosis for recovery to athletic activity depends onthe degree of proliferation, stiffness, and lamenessthat results from the injury; however, complete re-covery after the repaired fibrotic tissue remodels ispossible.131

Occasionally, the joint capsule will heal and thecollateral support will remain weak, so the liga-ments require surgical augmentation.132 The au-thor has used prosthetic replacement of thecollateral ligament with imbrication of the joint cap-sule over the prosthesis, which is an alternative thathas resulted in athletic soundness.

Supracondylar LysisSupracondylar lysis has been documented in theliterature and is correlated, in the racehorse, withlameness and in the yearling, with reduced perfor-mance.41 Supracondylar lysis is a radiographicfinding characterized by palmar/plantar bone ab-sorption and narrowing of the distal aspect of thecannon bone just proximal to the cannon bone ar-ticular surface of the fetlock joint when the fetlockjoint is viewed in a lateral-to-medial projection (Fig.41). It happens in the forelimb or hindlimb. Thehistologic appearance is one of hyperactive bonereabsorption.77

This radiographic sign is correlated with a reduc-tion in performance, but it is unlikely that it is thecause. The lysis occurs in an area of the palmar/plantar cannon bone where most of the vascularforamina enter the distal aspect of the cannon bone,but it is not part of the weight-carrying or support-ing ligamentous structure of the fetlock joint. Thisis an area of copious synovial villa that are involvedin removing debris and responding to trauma andinflammation in the fetlock joint.

Supracondylar lysis is a non-specific response toany insult that results in the significant and pro-longed inflammation seen after many different inju-ries. Its correlation with reduced performance is

probably more related to the primary injury thatcreates the inflammation and results in the lysisthan it is to the supracondylar lysis itself. Anytimethe synovial cul-de-sac of the palmar or plantar as-pect of the fetlock joint is chronically involved, bonereabsorption and narrowing of the distal aspect ofthe cannon bone occurs. In the yearling it is often asign of previous severe inflammation in the fetlockjoint from any of the significant neonatal diseases,including infectious arthritis or previous fracture.In the adult, it is usually a sign of chronic inflam-mation resulting from repetitive cyclic trauma.Therefore, when supracondylar lysis is encounteredradiographically, one should be most interested inidentifying the lesion(s) or site of inflammation thatcreated or is creating the lysis. Supracondylar lysisoccurs only palmarly and plantarly and is some-times incorrectly diagnosed at the dorso-proximalaspect of the fetlock articular surface. Demineral-ization dorsally is the result of impact damage fromhyperextension and the first phalanx impacting thedistal cannon bone with resultant erosion and demi-neralization or rarely, villonodular synovitis.

The primary disease that is causing the supracon-dylar lysis determines the prognosis. Many horseswith supracondylar lysis can perform well in spite ofthe radiographic finding if the causative insult hasbeen resolved and the joint has had a chance torecover. If the primary disease persists, the prog-nosis remains poor.

Fig. 41. This radiograph shows supracondylar lysis (arrow-heads) secondary to a chronic OCD of the sagittal ridge andcondyles of McIII.


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Foal Proximal Sesamoid Bone Fractures

There are few seemingly minor injuries in a foal oradult that have as many potential long-term conse-quences as a fracture of the sesamoid bone in a foal.Fractures of foal’s sesamoid bones are very common.Perhaps as many as 25% of all foals suffer some typeof injury to the sesamoid bone, most of which goundetected or are found coincidentally when exam-ining radiographs for some other reason. Mostfractures of the proximal sesamoid bone in the foal,when non-displaced, heal with little consequence tothe foal or the eventual adult athlete, but someinjuries, particularly if the continuity of the suspen-sory apparatus is damaged, can disable or limit ahorse’s athletic career before the horse is more thana neonate.133

A sesamoid bone by definition forms within a lig-ament and is normally located at a site where aligament must change a direction or traverse anangulation. In the horse, the proximal sesamoidbones form within the juvenile suspensory appara-tus. In the adult, there is a distinct difference be-tween the very elastic suspensory ligament and theinelastic distal sesamoidean ligaments.134 Thischange of biomechanics occurs at the sesamoidbones. The sesamoid bones in the neonate are notwell developed, and the suspensory ligament/distalsesamoidean ligaments are more contiguous; the lig-amentous support rather that the sesamoid bones isthe most important in maintaining fetlock joint an-gulation. In the juvenile, the sesamoid bone be-comes a greater component of weight bearing as itbecomes stronger, although it can be easily injuredbefore strenuous activity and the strengthening ofthe bone.

The most common predisposition to injury for afoal’s sesamoid bone is the young mare, often withher first foal, that is recently unburdened of the 200lb or so of pregnancy and feels the urge to race acrossthe field unimpeded. The neonatal foal is requiredto keep pace with the mare sprinting across the openfield; as the foal fatigues, it tries to maintain contactwith the mare, and the juvenile muscles are nolonger able to dampen the stress. With fatigue, thefoal fractures one or more of the sesamoid boneswithin the suspensory apparatus.133 It is verycommon that paired injuries occur, for instance, me-dial or lateral sesamoids in both forelimbs. Frac-tures of the hind sesamoids are much less common,because they are less vulnerable to fatigue than theforelimbs. Restriction of the mare to a confinedarea and gradual increase in exercise as the foalgains strength prevents the mare from exhaustingthe foal until it gets strong enough to sustain theexercise. It is important to allow foals exerciseearly to encourage muscular and skeletal develop-ment and coordination, but it should be restricted toa relatively confined area, gradually increasing tofield exercise as the foal grows.135 If a neonate orits mare requires restriction of exercise to a stall for

any reason early in life, graduating the return toexercise is critical to the prevention of sesamoidbone fractures.

Foal apical sesamoid fractures are often non-clin-ical and often discovered coincidentally if the foal oryearling is being radiographed for some other reason(Fig. 42). Apical sesamoid fractures rarely causelameness in the foal and generally heal withoutincident, but the sesamoid bone sometimes forms anon-union, even at this early age, because of thebiomechanics that impair bone healing in a sesam-oid fracture. These non-union apical fracturesneed to be dealt with before training, usually byremoval, but in the absence of lameness in the foal,they are not an urgent problem.

Mid-sesamoid fractures are less common in thefoal than the apical fractures. They almost alwaysheal spontaneously unless markedly displaced.The “tell-tale” result of a previous mid-sesamoidfracture is the elongated sesamoid (Fig. 43). Elon-gated sesamoids result from a displaced mid-sesam-oid or large apical fracture that has healed, fillingthe fracture gap as the healing process occurs.

Elongated sesamoids that are elongated proxi-mally with the base of the sesamoid in the normalposition are a predisposition to unsoundness, usu-ally sesamoiditis, and sometimes also refracturewith heavy training. The gap in the sesamoid bonethat fills in as the fracture heals disrupts the normalsuspensory ligament insertion. The fracture heal-ing with its attendant inflammation and the elon-gated sesamoid bone, which changes the angle ofloading of the suspensory ligament fibers on fullweight bearing of the fetlock joint, all predispose to

Fig. 42. This radiograph shows a chronic apical sesamoid frac-ture (arrow) in a yearling that occurred as a foal.


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inferior insertion strength of the suspensory liga-ment fibers. As more strenuous exercise is under-taken, the suspensory insertion begins to fail, andsesamoiditis/suspensory branch desmitis results.Mid-sesamoid and base sesamoid fractures are usu-ally accompanied by significant lameness initially,but the lameness normally resolves quickly if thestructural strength of the suspensory apparatus isnot lost (Fig. 43).

Abaxial and base sesamoid fractures with anydisplacement severely damage the foal’s athletic ca-reer.133 The abaxial sesamoid fracture detachessome or all of the suspensory ligament from thesesamoid bone, and the basilar sesamoid fragmentdetaches some or all of the distal sesamoidean liga-ments from the sesamoid bone (Fig. 44). Eithersituation is a severe threat to the foal’s athleticcareer.

Treatment of abaxial or base sesamoid fracturesin a foal is difficult; removal is not an option, be-cause it will assure disability of the suspensory ap-paratus. Reconstruction would theoretically bedesirable, but surgical implants have little to pur-chase in the fractured fragment of the sesamoid toreconstruct the sesamoid bone. The detached frag-ment is principally ligamentous with only a smallshell of bone. Normally, the foal must heal thefracture on its own.

If the fracture fragment separates from the parentbone and loses contact, a fibrous union develops, and

the foal’s athletic career is ended. If the base ses-amoid heals without proximal displacement of thesesamoid bone, base sesamoid fractures will likelybe functionally sound for most athletic pursuits.Abaxial sesamoid fractures are usually more devas-tating, because an abaxial injury normally pulls theentire suspensory ligament insertion away from theparent bone, detaching the support from the sesam-oid. These can heal, but rarely do they heal suffi-ciently to allow athletic activity.133 If they do heal,they are accompanied by marked sesamoiditis, andthe suspensory ligament insertion is rarely soundenough for high-speed exercise.

In general, sesamoid injuries in the foal result ininflammation during the process of healing thatcauses sesamoiditis, as defined by the enlarged vas-cular canals that are a marker for permanent dam-age to the suspensory apparatus and compromisethe function of the suspensory apparatus for the restof the foals life.39

A foal with a sesamoid fracture needs to be re-stricted until lameness and clinical swelling havesubsided. After the lameness and clinical swellinghave resolved, gradually increasing exercise is indi-cated. Normal care can be initiated if no distrac-tion and no lameness or pain on palpation persists.If the foal is lame or the sesamoid fracture is dis-tracted, then absolute confinement is imperative orloss of all chance of athletic career will occur. Afterthe bone has fully united, then gradually increasingexercise is appropriate. If the sesamoid fractureheals without change in shape of the sesamoid andwithout development of the enlarged vascular ca-nals, the sesamoid bone will be normal for futureperformance. If elongation of the sesamoid to asignificant degree in the proximal direction results

Fig. 43. This radiograph shows an elongated lateral sesamoid(bracket) as a result of a previous healed fracture.

Fig. 44. This radiograph shows a typical base sesamoid fracturein a foal.


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from the injury or if enlargement of the vascularcanals occurs as a marker of significant inflamma-tion at the suspensory/sesamoid insertion, then thefoal’s future athletic career will be compromised.39

The worst mistake that can be made with a foalwith a sesamoid fracture is to support the limb in acast or heavy bandage. The flexor tendons supportthe limb when the suspensory apparatus strength iscompromised by a sesamoid fracture. If externallimb support is used in foals, the flexor tendonsweaken. On removal of the external support, thelimb no longer has any structural support from theflexor tendons or the suspensory apparatus and thefetlock joint collapses, which further distracts thesesamoid fracture and risks total collapse of thelimb. Therefore, sesamoid fractures are best leftwith the limb unsupported. If the sesamoid boneinjury is biaxial or the collapse is present at the timeof injury, the prognosis is poor and hope for survivalwould require fusion of the fetlock joint.

Sesamoid Fractures in the Mature Horse

Fractures of the sesamoid bone in the adult are asomewhat different topic than fractures in the foal.Although the horse is still growing, sesamoid frac-tures that stay in close apposition have a reasonablygood chance of uniting. In the adult, after growthhas stopped, sesamoid fractures, other than veryfine fissures, almost never heal. These adult frac-tures do not heal, because they are exposed to theconditions favoring non-union of fractures. Ten-sion, lack of a periosteal blood supply, high motion,and continuous cyclic loading all mitigate againstfracture healing, and all are present in a fracture ofthe proximal sesamoid bone in the horse. There-fore, when active growth ceases, sesamoid fracturesrarely heal with a bone union, and a chronic non-union develops with its attendant inflammation andweak fibrous union.

The two fragments of a fractured sesamoid bonecontinually attempt to mount a secondary bone heal-ing response. This continual reaction to the insta-bility of the fracture and a progressive attempt tobridge the fracture are parts of the pathology thatpredisposes to lameness in a sesamoid fracture.Attempts at fracture healing in a sesamoid, just likewith a fragment in a joint, fail, because the strain istoo large across the fracture gap. The bone’s re-sponse is to open the fracture gap by demineraliza-tion of the fracture interface to reduce the shearstress. This progressive loss of bone further weak-ens the injured sesamoid bone.

Consequently, a weakened, inflamed, and demi-neralizing sesamoid bone suffers further progressiveavulsion of the ligamentous insertions. After liga-mentous attachments are weakened and fail, theycan never be reconstructed to the strength of theoriginal attachment. So, fractures of the sesamoidbone are particularly troublesome; they not onlydisable portions of the suspensory apparatus by de-taching the fracture fragment from the parent bone,

but additionally, they progressively weaken the par-ent bone, predisposing to loss of additional suspen-sory or sesamoidean ligament attachment duringthe healing process.

To neutralize sesamoid fracture’s natural at-tempts to heal, one must either negate the motionthat occurs between the two fragments of bone tofacilitate healing or eliminate one of the fragmentsof bone to stop the healing process. With smallfragments, the treatment of choice is to remove thefractured fragment and stop the healing response bythe parent bone to preserve the remaining normalligamentous insertions. With large fractures, suchas mid-sesamoid fractures where elimination of oneof the fragments of the bone would compromise theintegrity of the suspensory apparatus, reconstruc-tion of the bone is the only alternative.

Axial Sesamoid Fractures

Axial sesamoid fractures are rare and are generallyseen in the presence of a distal cannon bone condylarfracture.136 They occur when the normal joint me-chanics are disabled by the unstable condylar frac-ture. As weight is applied and the displacedcondyle is pushed dorsally, the ipsilateral sesamoidis displaced dorsally and the intersesamoidean lig-ament is bent over the disrupted interface of theparent cannon bone at the fracture site. This re-sults in fracture of the axial aspect of the sesamoidbone that articulates with the injured condyle.

There is no treatment for this fracture; it is acareer-ending injury, even if the displaced condylarfracture is reconstructed and heals perfectly, be-cause the intersesamoidean ligament injury that re-sults from an axial sesamoid fracture causes chroniclameness and does not heal.136 Occasionally, axialsesamoid fractures will be seen spontaneously with-out a predisposing condylar fracture (Fig. 45).

Reconstruction of the condylar fracture results ina breeding animal, but the lameness caused by theaxial sesamoid fracture in a broodmare or stalliontakes as long as 1 yr to resolve whether or not froma predisposing condylar fracture or spontaneousfracture (Fig. 45). These fractures can be ex-tremely troublesome; the horse walks reasonablywell after the condylar fracture has been replacedand stabilized surgically, but it is uncomfortable forthe horse to stand with tension on the axial sesam-oid fracture with or without a condylar fracture.Some horses will be lame for many months. Stallrest is more painful than walking, so paddock exer-cise should be maintained or initiated as soon as thecondylar fracture repair will allow. The long-termprognosis for a breeding animal is favorable.

Apical Sesamoid Fracture

Apical sesamoid fractures from one-fourth to one-third of the volume of the bone are common frac-tures in all breeds of racehorses (Fig. 46).137 Theyare infrequent in horses of lesser use levels. Theexplanation for this was elucidated in research,


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which found that training caused the suspensoryligament to become stronger to a greater degree andat a more rapid rate than the sesamoid bone, mak-ing the sesamoid bone the weak link in the high-speed athlete.134

Apical Sesamoid Fractures Occur Primarily in the RacingBreedsIt has been postulated that an area of differentialremodeling located at the proximal one-third to one-fourth of the sesamoid bone predisposes it to frac-ture, although there is information to both supportand refute this concept.138 There is good informa-tion that the location of the fracture is relativelyconsistent, suggesting that an apical sesamoid frac-ture is not a haphazard occurrence.

Acutely, fractures of the sesamoid bone causelameness, which gradually abates and even becomestolerable in some horses. Eventually, in high-levelathletes, the mobile apical fracture begins to pro-duce the inflammation caused by the healing re-sponse of the parent bone and begins to weaken theremaining normal suspensory ligament fibers thatinsert into the parent sesamoid bone. It is the pres-ervation of these fibers that is the goal of treatmentof an apical sesamoid fracture. After the sesamoidfracture occurs, it is the remaining normal suspen-sory ligament that supports the horse’s athletic ac-tivity, because the suspensory ligament fibers that

are attached to the fracture fragment are detachedfrom the distal aspect of the suspensory apparatus.Sesamoid fractures are a disease of the suspensoryapparatus and not the fetlock joint itself, becausethey rarely lead to any significant degeneration ofthe joint; rather, they cause lameness through theireffects on the suspensory apparatus.

Because an apical sesamoid fracture in a maturehorse will never heal, surgical removal is the treat-ment of choice and in fact, was the first articularsurgery described in the horse.137,139 Surgical re-moval preserves the normal parent sesamoid boneas well as the remaining suspensory ligament at-tachment from progressive fiber loss caused by thehealing response provoked by the apical sesamoidfracture.

Although removal of apical sesamoid bone frac-tures through an open incision was a common andsuccessful surgical procedure for some period oftime, the preferred treatment is now arthroscopicremoval.140 Currently, the open incision has beenreplaced by arthroscopic extraction of the apicalfragments in almost all instances because of thereduced morbidity to the fetlock joint. The progno-sis has been well defined in both the Thoroughbredand the Standardbred, and it is favorable for apicalsesamoid fractures as a group.140,141 Further re-finement of the prognosis was recently published ina paper that compared the different locations withinthe horse with the prognosis.142,143 Apical sesam-oid fractures of lateral sesamoid bones in the fore-limbs and all four sesamoids in the hindlimbsroutinely have an excellent prognosis for returningto pre-injury level in adults and achieving perfor-mance levels comparable with uninjured siblings injuvenile horses, if they are removed arthroscopi-

Fig. 46. This radiograph shows an apical sesamoid fracture(arrow).

Fig. 45. This radiograph shows a spontaneous axial sesamoidfracture without a predisposing condylar fracture (arrows).


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cally. But, a medial apical sesamoid fracture of aforelimb, in both adult and juvenile horses, carries�one-half the prognosis for a hindlimb apical sesa-moid fracture or a lateral sesamoid fracture in aforelimb. The marked difference, present both inthe unraced and raced individuals, seems to be re-lated to the anatomy and the importance of themedial sesamoid bone in the forelimb.

Careful examination of each individual apical ses-amoid fracture can further refine the individual in-jury prognosis. As a rule of thumb, the prognosisdeclines as the suspensory ligament involvementincreases. Suspensory ligament injury occurs fromthe fracture and from concurrent suspensory liga-ment desmitis. Concurrent suspensory ligamentdesmitis decreased the prognosis.143 So, refine-ment of the prognosis for an apical sesamoid frac-ture can be done using radiographic estimates orultrasound measurement of the suspensory liga-ment involvement.

Post-operative rehabilitation of the horse with anapical sesamoid fracture is routinely assessed by theexamination of the suspensory ligament before re-sumption of training is desired. In the author’shospital, horses with apical sesamoid fractures andno suspensory ligament damage are examined at 4wk post-surgery with an ultrasound exam, and if thesuspensory ligament is not inflamed other thanwhere the fragment was removed, exercise isreinitiated.142

Articular Abaxial Sesamoid Fractures

Articular abaxial sesamoid fractures are generallysimilar to apical sesamoid fractures in their assess-ment and treatment (Fig. 47). They occur withinthe heart of the suspensory ligament insertion, so asmaller fragment of bone damages a larger amountof suspensory ligament insertion than with an apicalsesamoid fracture.144

The prognosis is determined by the amount of sus-pensory ligament loss created by the sesamoid frac-ture and any attendant suspensory ligament injury.Frequently, there is significant suspensory ligamentdamage, and the guarded prognosis reflects this diffi-cult concurrent injury.144 Arthroscopic removal issimilar to removal of the apical sesamoid fracture insurgical technique and aftercare.

Mid-Sesamoid Fracture

Mid-sesamoid fractures in the mature horse are adifficult problem, because they totally detach one-half of the suspensory apparatus from the distalsesamoidean ligaments (Fig. 48). Removal of afragment nearing one-half of the mass of the sesa-moid bone simply assures no hope of reconnectionbetween the components of the suspensory appara-tus. Therefore, the only potential salvage for ath-letic activity is to attempt fixation and achievereunion of the two halves of the sesamoid bone.Without fixation, displaced mid-sesamoid fractureshave no chance to heal after the horse is mature.

The reasons for the occurrence of a mid-sesamoidfracture have not been well elucidated. Certainly,some fractures are accompanied by sesamoiditis,demineralization, and loss of strength of the sesam-

Fig. 47. This dorsal oblique “skyline” radiographic projection ofthe abaxial surface of this sesamoid bone shows an articularabaxial sesamoid fracture (arrow).

Fig. 48. This radiograph shows a mid-sesamoid fracture.


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oid bone, making it likely that the structural dimi-nution and diminished strength predispose the boneto fracture. However, many sesamoid bone frac-tures have no apparent predisposition for their oc-currence, and the explanation for failure of aradiographically normal sesamoid bone is un-clear.111,145 The best information shows that con-tinuous high-level stress over a long period of time ishighly correlated to the occurrence of mid-body ses-amoid fractures, but why a particular sesamoid frac-ture occurs is still unclear.146

The treatment through internal fixation can bedone in two principal ways: the use of screws orwires, one or multiple, to adapt the bone fragmentsor to reconnect the bone.147 In most instances, abone graft is added to the fixation to stimulate re-pair because of the poor biomechanics of sesamoidfracture healing. Lag-screw fixation can take placefrom the apex, the base, or the abaxial surface, de-pending on the configuration of the fracture.148

The lag screws are inserted in normal A-O fashion,and it is the author’s preference to coapt the sesam-oid bone, insert the screw, and then subsequentlyloosen the screw to insert the bone graft, although itcan be done in any order.

The surgical procedure is technically challengingbecause of the interposition of the foot into the loca-tion where one would like to orient the drill to createthe hole; the fracture is best reduced in flexion, butthe surgery is easiest with extension of the fetlockjoint. In addition, the healing process is fraughtwith many potential difficulties. In addition to thelimited bone to insert the fixation, the bone healsslowly, and if the healing process is accompanied bysignificant sesamoiditis, as it usually is, even a per-fect reduction and healing of the sesamoid bone maynot result in a sound horse. Wire fixation can sim-ilarly adapt the two portions of the sesamoid bonelike the screw, and a wire is easier to insert but hasbeen shown to be less likely to result in an athletethan lag-screw fixation.148,149

The prognosis for successful treatment of mid-sesamoid fractures is limited by the technicaldifficulty and the probability of subsequent sesam-oiditis. Repair is normally attempted only inhorses that have no use other than their athletecareer. Although many horses can return to rac-ing, it is difficult to keep them sound because of thesesamoiditis that is caused by the fracture and thehealing process.148

Base Sesamoid Fractures

There are two distinct categories of base sesamoidfractures. The most common category is the basesesamoid fracture that is predisposed by the changein shape of the distal metacarpus caused by palmardistal cannon bone degeneration. The flattening ofthe distal palmar aspect of the metacarpus and thealteration of the congruency of the articular surfaceof the sesamoid bone with the distal cannon boneresult in abnormal stress concentration and fracture

of the base of the sesamoid. These fractures ofteninvolve the entire width of the base of the sesamoid,are normally a thin portion of the base of the sesa-moid bone, and frequently are comminuted.150,151

Treatment is unrewarding for these secondaryfractures of the base of the sesamoid bone. Theyare impossible to fix, and removal detaches signifi-cant sesamoidean ligament insertion. However,more importantly, even if the fragment is small,surgical treatment of the base sesamoid fracture istreating only a result, not the primary disease,which is the ongoing degeneration of the palmaraspect of the metacarpus. This degenerativechange is a career-ending injury in the horse, sosurgical treatment is not normally elected.

Small base sesamoid fractures that are not accom-panied by palmar flattening of the distal aspect ofthe metacarpus can be treated with arthroscopicremoval (Fig. 49).150,151 It is preferable to have lessthan one-half of the width of the sesamoid boneinvolved in one of the two dimensions, dorsal topalmar/plantar or medial to lateral, to be successful.If the middle portion of the sesamoid bone is in-volved in the base sesamoid fracture, then the im-portant middle distal sesamoidean ligament hasbecome involved, which decreases the prognosis.However, fractures of the base of the sesamoid thatinvolve only the dorsal margin and therefore, theshort or cruciate sesamoidean ligaments have a fa-vorable prognosis with removal.150,151

Arthroscopic removal is similar to the surgicalprocedure used for the removal of fracture frag-ments of the palmar/plantar aspect of the first pha-lanx with two arthroscopic portals and dissection tofree the fragment before removal.

Fig. 49. This radiograph shows a base sesamoid fracture (arrow)without palmar cannon bone flattening.


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Non-Articular Abaxial Sesamoid FragmentsAbaxial sesamoid fractures that are non-articularpresent a somewhat different problem (Fig. 50).Large fragments that detach large numbers of sus-pensory insertion fibers are not amenable to surgicalresolution. However, horses with small fragmentsthat detach only a small portion of the suspensoryligament insertion may benefit from fragment re-moval, because the unstable fragment provokes thesame healing response as does an articular fracturefragment that involves the abaxial aspect of thebone, which further damages the suspensory liga-ment. The healing process continually inflamesand softens the parent sesamoid, allowing progres-sive loss of more suspensory ligament fibers. Someof the smaller abaxial sesamoid fragments withinthe suspensory ligament are tolerated without a re-sponse by the parent bone. If the parent bone is nottrying to heal the fragment, then it is likely best leftundisturbed. But, most unstable fragments con-tribute to progressive loss of suspensory ligamentanchorage and eventually, permanent lameness byprovoking a healing response by the parent bone.These fragments should be considered for removal.

One must be cautious and use judgment in recom-mending removal, because if the sesamoid fragmentis quiescent and not stimulating a response by theparent bone, the surgical invasion that sacrificessuspensory attachment may be worse than the dis-ease. So, judgment is important, but in most in-stances when high speed exercise occurs with asesamoid fragment in place, the sesamoid bone re-sponds and attempts to heal the fragment. This isaccompanied by the lucency and demineralization

that further compromises the strength of the sus-pensory ligament/sesamoid bone insertion. If al-lowed to continue, the horse seldom stays sound, soelective removal before permanent disability is acritical decision.

These fracture fragments involve the suspensoryligament insertion but are not directly accessible forarthroscopic removal. Therefore, some suspensoryligament must be sacrificed if the fragment is to beapproached. The shortest distance to the fragmentwith the least suspensory disruption is the approachof choice. In some instances, the arthroscope canbe used to make an incision in the suspensory liga-ment through the joint and access the fracture frag-ment from that aspect; in other instances, directaccess of the fracture fragment through the abaxialsurface of the suspensory ligament does the leastdamage.

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