This document discusses the anatomy, biomechanics, pathogenesis, diagnosis and treatment of cranial cruciate ligament disease in dogs. It provides details on the cruciate ligaments and menisci, how injury typically occurs from trauma or degeneration, common clinical signs, and traditional surgical techniques for repair or reconstruction. Current trends focus on techniques that better restore normal joint kinematics, such as intra-articular reconstruction and use of isometric graft placement. Meniscal injury often accompanies cruciate ligament rupture and removal can accelerate osteoarthritis.

1. “101 ways to fix a
Cruciate”
Stephen M Fearnside
Veterinary Surgical Specialist
Small Animal Specialist Hospital
sfearnside@sashvets.com

3.  Design: Multicentre
prospective comparative
study
 “in the absence of a
cohort of willing oxen as
a control group” ……..
 Chose to compare
intelligence test scores
and dominant hand grip
strength in ortho
surgeons (x36) and
anaesthetists (x40)
 3 UK District General
Hospitals
VS

5. Introduction
• Incidence of CrCL disease in the USA in
dogs exceeds that in humans (Helliker,
Wall St Journal 2006)
• Estimated repair costs in USA (2003)
are $1.23 billion annually
• Recent studies demonstrate that no
single technique returns patients to
normal function consistently

6. Summary
 Anatomical considerations
 Biomechanical analysis
 Review of Pathogenesis
 Review of traditional techniques
 What about the poor old meniscus?
 Current trends and issues

7. Anatomy
 Diarthrodial joint
 2 distinct articulations
1. Femoral-tibial
2. Femoropatella
 Joint Capsule:3 distinct
interconnecting
cavities. Reinforced by
fibrous retinaculum,
local ligaments and
tendons

8. Menisci
 Semilunar fibrocartilages
 Cranial and caudal
meniscotibial ligaments
 Meniscofemoral ligament
(lateral meniscus)
 Intermeniscal ligament
 Blood supply –
peripheral 10-15%
 Function: stress transfer,
joint stability, lubrication,
proprioception (horn
innervation)
Lateral
meniscus
Medial
meniscus
Intermeniscal
ligament

9. Ligamentous support
 Primary support via femorotibial ligaments:
1. Cruciate ligaments
2. Medial and lateral collateral
ligaments.

10. Cruciate Ligaments
 Blood supply – from
synovial tissue sheath,
fat pad, caudal joint
soft tissue.
 Intra-articular but
extrasynovial
 Primary stabilisers
against cranial/caudal
tibial translation, axial
rotation (twisting on
each other),
hyperextension and
excess valgus/varus in
flexion.
Cruciate ligaments’
blood supply

11. Cranial Cruciate Lig
 Origin = caudomedial
aspect of lateral femoral
condyle
 Insertion = cranial
intercondyloid area of tibia
 2 functional componants
1. Craniomedial band
2. Caudolateral band
 Ligament spirals laterally
approx 900
 collagen bundles grouped
into fascicles –
tightening/relaxing through
motion.
Craniomedial
Band
Caudolateral
Band

12. Stifle Joint Motion
 Flexion and extension in sagittal plane
 Slight cranio-caudal movement – not uniplanar
motion
 Secondary restraints to cr-ca motion = joint
capsule, menisci, collat ligs, articular surface
shape, muscle forces
 “Screw-home” mechanism

13. Stifle Joint Motion
Cranial Tibial Thrust
 Result of ground
reaction forces +
extensor muscle forces
= compressive forces
through tibia shear
force generated
 Countered by CrCL
(passive restraint) and
hamstrings/biceps m
(active restraints)

14. Pathogenesis
“rupture of the cranial cruciate
ligament is seen for the most
part in active jumpers, and
especially in those individuals
having the defect in
conformation where stifle and
tarsus are carried in over-
extension. The absence of
normal flexion angle of these
joints in the standing position
appears to be a predisposing
cause”
Erwin Schroeder, 1939

15. Pathogenesis
Trauma
 20% cases
 Cranial tibial thrust
mechanism – eg
jumping. Magnitude of
thrust > breaking
strength of ligament
 Excessive internal
rotation
 Hyperextension

16. Pathogenesis
Degeneration
 Age related changes in ligament (Vasseur et al, 1985).
 Stress/strain energy of ligament decreases with age
 Age related changes significantly greater for dogs>15kg
 Histological changes
 Tissue changes identified during progressive rupture (Muir et al
2002, Vasseur et al 1985)
 Loss of ligament fibroblasts
 Transformation of fibroblasts to ovoid or spheroid phenotype
 Disruption of normal type I collagen – loss of crimp, disruption of
fascicles
 Contribution of blood supply
 Bilateral disease – 37% within average 17months (Doverspike
et al, 1993)
 Young large breed dogs - <4ys, Rottweilers over
represented. Postulated cause = inadequate exercise when
young?? (Bennett et al, 1988)

17. Sagittal section
through cranial
cruciate ligament
demonstrating
chondroid
metaplasia of
fibroblasts and
failure to maintain
collagen fibrils

18. Pathogenesis
Conformation
 Contributing factors = internal rotation,
hyperextension, tibial plateau slope
 Young large breed dogs -Read & Robins (1982)
 Small breed dogs – Macias et al 2002, Selmi &
Padhilla 2001
 Medial patella luxation
 Congenital narrowing of the intercondylar notch

19. Pathogenesis
Immune mediated joint disease
 Plasmacytic lymphocytic synovitis (Galloway &
Lester, 1995).
 Anticollagen antibodies in serum and synovium
(Nierbauet et al 1987, DeRooster et al, 2000)
 The chicken or the egg???
Osteoarthritis
 OA a primary lesion?? (Hulse & Aron, 1994).
 Role of genetics and conformation.

20. Epidemiology

21. Epidemiology
 Breed: large breed dogs predisposed
Rottie, Newfowndland, SBTerrier (Whitehair & Vasseur,
1993)
N.Mastiff, Retriever, Labrador, SBTerrier (Duval et al,
1999)
Breed variation in physical properties – Rottie ligament
requires ½ load per unit body mass that the GH ligament
requires to rupture (Wingfield et al, 2000)
Comparison of TPA between clinically normal GH and
Labradors with and without cruciate lig disease (Wilke et
al 2002).
 Body Size: <22kg lower prevalence (Whitehair et al 1993)
<15kg tend – degenerative changes occur later in life
(Vasseur et al, 1985)
 Obesity = increase load.

22. Epidemiology
 Sex: Whitehair & Vasseur, (1993) reported higher
prevalence in neutered and female dogs
Duval et al (1999) increased risk in desexed dogs
but no male/female difference.

23. Clinical Signs and Diagnosis
 Gait assessment: reducing external limb load, limb carried in
greater flexion (Vilensky et al 1994, Korvick et al 1994)
 Joint effusion
 Cranial draw and tibial compression (mimics loading to elicit
cranial tibial thrust)
What % of patients have drawer????? (Carobbi &
Ness 2009)
 Radiography – Degenerative joint disease
 effusion,
Compression stress radiography (de Rooster & Van
Bree 1999)
 Joint fluid analysis: WCC<5000/mm3
, mononuclear cells
predominate.

24. Radiography

25. Treatment
Conservative management
 Cats – mean follow-up 20.5 months all cats (n=18) clinically
normal. Mean time to normal function 4.8wks (Scavelli &
Schrader 1987)
 Small dogs <15kg :
90% success rate if <20kg (Pond & Campbell 1972).
 86% clinically normal or improved after mean f/up 36.6mths
(Vasseur, 1984).
 73% (8/11) free of lameness after mean 5.5mths (Strande
1967)
 Dogs >15kg: 81% of dogs had persistent or worsening
lameness after mean f/up 10.2mths (Vasseur, 1984)

26. Surgical Management
 Methods of conventional repair:
1. Primary repair – only for avulsion
injuries.
2. Intra-articular or intra-capsular repair
3. Extra-articular or extra-capsular repair.

27. Intra-articular reconstruction
 Graft selection:
 Biological tissue
(autograft, allograft,
xenograft)
 Synthetics eg goretex,
dacron, braided
polyester
 Combination
(composite grafts)
 Graft Placement:
isometric points of
attachment to maintain
graft length through
ROM.

28. Graft issues
 Arnoczky et al 1982:
• Patella tendon graft revascularisation by 20 weeks –
vulnerable during the first 20weeks
• Initial necrosis revascularisation remodelling
• Revascularisation from: fat pad, posterior synovial
tissues
• 12mths = vascular and histological characteristics of
normal ligament
 Biomechnical studies:
• Material properties decline significantly after
implantation
• Ultimate stiffness and load <35% of original ligament

29. Extra-articular reconstruction
 Quicker, easier (except fibula head
transposition)
 Changes the ‘instant centre of
motion” of the stifle which results in
compressive forces at the tibio-
femoral contact points (Arnocsky et
al 1977)
 Designed to rotate tibia externally
allowing the MCL to act
synergistically with the laterally
placed suture to inhibit draw. Stifle
therefore becomes “hinge joint”
altering stifle kinematics (Patterson
et al 1991)
 Ultimate joint stability due to
periarticular fibrosis.

30. Isometry
“For a suture that spans a joint to provide
support without limiting range of motion, its
attachment points on either side of the joint
must remain the same distance from each other
from full extension to full flexion”
Roe et al, VCOT 2008

31. Isometry: Roe et al VCOT 2008
Most isometric = Tibia site:1,2,5 if
femoral anchor site 4 used

32. Materials
 Braided non-absorbable suture
material – draining sinus tracts
reported in 21% cases.
 Monofilament nylon leader
line
 Orthofibres
 Sterilisation
 Knotting vs crimping –
 Crimping shown to result in less
elongation (knots tend to slip)
but also reduces strength
(Sicard et al 2002).
 Crimping superior in all
biomechanical assessment
parameters (Anderson et al,
1998)

33. Instrumentation

34. Materials – transcondylar systems
 Tightrope CCL
 Securos
systems:
• XGen CCR
• Bone anchors
and orthofibre

35. Results
 Postoperative results: 85-90% improve. Complete
soundness = Less than 50% (Moore & Read, 1996).
 Studies evaluating factors that influence prognosis
found that surgery type had little influence (Fallon &
Thomlinson 1986, Moore & Read 1995)
 Studies report that DJD progresses despite
satisfactory clinical results (Vasseur & Berry 1992)
 Biomechanically intra-articular techniques more
consistent with normal state using “instant centre of
motion” model (Arnoczky et al 1977) – the future??.

36. Meniscal Injury
 Incidence varies – low
frequency for partial ruptures
(25% reported by Scavelli et all
1990) up to 80% in some
reports with complete tearing of
CrCL
 Vascular supply – outer 10-
25%
 Mechanism of damage –
crushing injury during cranial
subluxation of tibia
 Lesion classification – 7
types (Bennett & May, 1991)

38. The Meniscus
 Human studies suggest that degree of
degenerative change directly proportional to
amount of meniscus removed (Cox et al
1975).
 Meniscal release – controversial. Simple
transection has been shown to result in loss
of load bearing capacity – loss of ability to
resist circumferential strain.

39. Management of meniscal
injury
 Healing potential –
peripheral tears, radial
tears
 Experimental techniques –
vascular access channels,
exogenous fibrin clots,
allograft, prosthesis.
 Porcine small intestinal
submucosa implants –
Welch et al (2002), Cook et
al (1999).

40. Tibial Plateau Leveling Osteotomy
 The Slocum approach:
1. Slocum B, Devine T. Cranial tibial thrust: a primary force
in the canine stifle. JAVMA, 183:456, 1983
2. Slocum B, Devine T. Tibial plateau leveling osteotomy for
eliminating cranial tibial thrust in cranial cruciate ligament
repair. JAVMA, 184:564, 1984.
 Procedure does not attempt to restore
function, but rather provide stability during
weight bearing by reducing cranial tibial
thrust
 Note – does not eliminate passive drawer!!

41. Determining the
tibial plateau angle (TPA)
 True lateral of stifle (femoral
and tibial condyles
superimposed).
 Tibia parallel to table top
 Slope of medial tibial plateau
determined
 Tibial functional axis
determined
 TPA defined as angle between
slope of the medial tibial
condyle and the perpendicular
to tibial long (functional) axis.
Tibial long
axis
Medial tibial
plateau
Perpendicular
to long tibial
axis
TPA

42. Procedures
 Slocum Technique –
patented
 Meniscal release –
recommended to allow
caudal pole of medial
meniscus to remain in
caudal compartment of
joint during cranial
translation of tibia.
 Medial arthrotomy –
routine or limited
caudomedial approaches.

43. T.P.L.O

45. T.W.O

48. P.T.I.O.
Proximal
tibial intra-
articular
osteotomy

49. Chevron
Wedge
Osteotomy

50. T.T.O.
Triple
Tibial
Osteotomy

51. T.P.L.O +
Cranial
Tibial
Wedge
Osteotomy

52. T.T.A.
Tibial Tuberosity
Advancement

53. So where do we go from
here?
Initially I think we need to slow
down!
Rob McCarthy JSAP 2009

54. Thoughts on TTA

55. TTA – “the
beginning”
Cranialisation of
the tibial
tuberosity

56. Thoughts on TTA
 Case selection
 Newer systems
 To graft or not to
graft?
 Stifle mechanics
 Meniscal release?
 Complications
 Outcomes

57. TTA Complications

58. TTA
Complications

59. 1 week postop

61. TTA modifications – “Archie”
 WHWT
 Partial cruciate
tear
 Modified
Marquet
technique

62. Archie

63. Medial Patella Luxation
Kyon
Washer/S
pacer
XGEN
Securos

65. TTO – “Vader”
35 degrees

67. Postoperative rehabilitation – the
forgotten science?
 Marsolais et al 2002: Prospective clinical trial with 51
dogs.
Limb function evaluated before and after surgery using
force plate analysis
Dogs assigned into rehabilitation or exercise restriction
groups.
Rehab programme – leash walking, massage, passive
ROM, swimming.
Significant increase in limb usage in rehab gp
compared with exercise restricted gp at 6mths.

68. “My Opinion – for what it is worth ”
 Cruciate surgery in the dog = strong
opinion based on weak data.
 A good extracap = a good TPL
surgery……BUT
 TTA provides a more consistently good
outcome in large breed dogs
 Small breeds????
 Going forward with extracap – focus on
isometry.

69.  Inspect the joint - Resect damaged
ligament and meniscus – controversial!
 Adhere to strict aseptic principles.
 Antibiotic use
 Don’t over-tighten extracap sutures –
achieve stability
 Rehabilitation is important!

70. The unanswered questions
 There are many!!!
 Preventative strategies remain in their infancy
 If TPL restore mechanical stability then why does DJD
progress?
 Why do only 60% of dogs with confirmed CrCL disease
have drawer
 Why are we seeing so many cases of CrCL disease
 What role does genetics play – shown to play a role in
Newfies (Wilkie et al, 2006)

71. The Future??
 Lars Ligament

72. Stifle Joint Replacement
 We have the
technology!!!
 Long recovery times
 Complicated and
challenging surgery
 Case selection!

74. Tables
Table 1 Participants’ demographics, intelligence, and grip strength
Characteristic Orthopaedic surgeons (n=36) Anaesthetists (n=40)
Mean (SD) age (years) 42.2 (8.82) 42.5 (8.63)
Grade—consultant:specialist registrar 20:16 21:19
Handedness—right:left 36:0 38:2
Mean (SD) intelligence 105.19 (10.85) 98.38 (14.45)
Mean (SD) grip strength (kg) 47.25 (6.95) 43.83 (7.57)

75. Study Conclusions
The stereotypical image of male orthopaedic
surgeons as strong but stupid is unjustified in
comparison with their male anaesthetist counterparts.
The comedic repertoire of the average anaesthetist
needs to be revised in the light of these data.

76. The author’s recommendations:
“we would recommend caution in making
fun of orthopaedic surgeons, as unwary
anaesthetists may find themselves on the
receiving end of a sharp and quick witted
retort from their intellectually sharper
friends or may be greeted with a crushing
handshake at their next encounter”.

77. Clinical Update – Wound Therapy using
PICO (Smith & Nephew)

78. PICO – Negative pressure for wound
therapy
 Single use negative pressure
wound therapy system
 Provides -80mm Hg negative
pressure to wound bed
 7 day use, 2 dressing per pack
 Dressing consists of:
 Silicone adhesive contact
layer
 Airlock layer that
distributes –ve pressure
evenly
 Absorbent layer
 High MVTR that allows
excess fluid to transpire

79. Advantages of NPWT:
 Promotion of closed moist
wound environment
 Reduction of tissue oedema
 Enhances wound contraction
 Mechanical stimulation of
wound bed
 Stimulation of angiogenesis
and alteration of blood flow at
wound edge
 Aids in GT formation
 Physical splinting of wound
and aids graft adherence.

80. “Ashleigh”
Grade II MCT
right
antebrachium