AN OVERVIEW OF PATELLAR LUXATION
Patella luxation or femoropatellar instability is a common cause of lameness in dogs. There are varying degrees of the
abnormality from a mild instability within the trochlear groove to a complete, irreducible luxation of the
patella. Clinical lameness associated with the various degrees may range from intermittent clinical signs to
permanent lameness. The direction of the luxation maybe in the medial or the lateral direction. Patella luxation has
been reported to be heritable or traumatic in nature. The most common form of the disorder is the heritable or
developmental medial patellar luxation in the small breed dogs. Lateral luxation in small dogs is rare and is usually
heritable. Lateral patellar luxation in large or giant breed dogs is often a distinct syndrome associated with severe
limb deformities and carries a guarded prognosis. The incidence of patella luxation in large breed dogs is increasing.
Felines, also, have been reported to be affected by patellar luxation, but not as frequently as the dog. A grading
scheme is utilized to standardize
of the disorder. (Table 1)
cases the luxation is not present at birth. The anatomical deformities that cause the luxation are present at birth.
Medial luxation is more common than lateral luxations in all of the breeds.
Medial luxation accounts for 75-80% of the luxations.
Bilateral luxations are seen in 20-25% of the cases.
The normal anatomy and function as well as the interrelationships of the entire rear limb ( hip joint, femur, stifle,
and tibia ) must be understood before the abnormal state can be appreciated. (FIGURE 1) Normal angulation for the
hip joint has been established in three different planes. From the lateral view, the cranial flexor angle of the hip is
normally 110 degrees. (FIGURE 2) The flexor angle of the stifle is 130 degrees. From the craniocaudal view,
the femoral neck to shaft angle is 130 degrees. (FIGURE 3) An increase in this angle makes the stifle shift outwards
into a stance know in lay terms as bow-legged or coxa vara. A decrease in the angle is knock-kneed or coxa valga.
From the stifle joint looking-up from the end through the shaft of the femur, the femoral neck should form an
angle of 0 degrees at birth and approximately 27 degrees when mature. (FIGURE 4) The proper anatomic alignment
is necessary for stability of the stifle joint and the proper functioning of the extensor mechanism.
The extensor mechanism of the stifle is comprised of the quadriceps muscle group
( rectus femoris, vastus lateralis, vastus intermedius, and vastus medialis),
patella, trochlear groove, straight patellar ligament, and the tibial tuberosity.
It is embedded in the tendon of the quadriceps muscle. Articulation with the trochlear cartilage is necessary for
maintaining the nutritional integrity of the surrounding cartilage. The patella allows for even tension when the stifle
is extended and also acts as a lever arm. The human quadriceps requires 15-30% increase in contractile force without
the patella. The patellar ligament is the single confluence of the quadriceps tendon distal from the patella
to the tibial tuberosity (tubercle, crest). The tuberosity is located cranial and distal to the condyles.
There is a specific alignment of the quadriceps, patella, trochlea, patellar ligament and tibial tuberosity for proper
functioning. A deviation in any of the components will result in a tension that predisposes to luxation of the patella.
abnormalities is, in part, dependent on the severity of the disorder and the age of the animal during the severe
stage. A significant potential for axial and torsional growth is present in the cartilage columns of the growth plate
(physis) of the distal femur. With medial luxation there is a lateral torsion of the distal femur.
The origin of the deforming force is still uncertain. Two theories have been proposed; one of a persistence
of anteversion at the hip joint (investigated experimentally) and the other of a modifier gene that selectively acts
in a specific anatomic region at a critical stage of embryogenesis (speculative).
displaces the origin of the quadriceps muscle group medially in relation to the long axis of the femur.
The internal rotation displaces the tibial tuberosity medially. These result in a medial displacement of the
quadriceps muscle group relative to the long axis of the femur. Contraction of the quadriceps along a straight line
from the displaced origin to the tibial tuberosity results in the medial displacement of the patella.
growth plate, which retards growth. A decrease in pressure applied parallel to the growth plate will accelerate
growth. The degree of lateral bowing depends on the grade of patellar luxation and the age of the patient at
the onset of luxation. Abnormal growth will continue as long as the patella is luxated medially and the growth plate
is active. In the adult dog, existing bone responds to stress by increased bone deposition and realigns according
to stress (Wolff's Law). This is remodelling and is much slower that growth plate deformation.
Deformity may occur through remodelling, but this requires a long period of time. More typically,
in the mature dog abnormal forces maybe manifested by an increase thickness of the trabecula on
the medial aspect of the stifle.
The response to an increase or decrease of pressure at the metaphyseal growth plate is similar to that of
the physis (increase in pressure results in a decrease in growth, the converse also being true).
The articulation of the patella within the trochlear groove exerts a physiologic pressure on the
articular cartilage that retards cartilage growth. This continued pressure by the patella is responsible for
the development of normal depth of the trochlear groove. The degree of deformity depends on the grade
of luxation (the amount of time the patella is luxated) and the age of the patient at the onset of luxation.
The degree of abnormality varies from nearly normal trochlear depth to the absence of a trochlear groove.
of the articular cartilage. The same mechanism of presence or absence of pressure will result in a
hypoplastic medial condyle when the patella is luxated medially. The increase in pressure can arises from
the forces created by medial malalignment of the extensor apparatus or by a shift in the weight-bearing axis
toward the medial direction resulting from lateral bowing of the distal femur. Subsequently the lateral condyle
is elongated from accelerated growth.
The deformities associated with a medial patella luxation are medial displacement of the tibial tuberosity,
medial bowing of the proximal tibia, and lateral torsion of the distal tibia. The proximal tibial aberrations
are from the mechanism previously discussed- the increase or decrease of pressure on the growth plate with
a resultant deviation in the longitudinal axis of the bone. The persistent anteversion and internal rotation of
the limb causes a compensatory rotation of the foot. In order for the foot to be placed properly,
the dog must externally rotate the tarsal joint, which results in external torsion on the distal tibial growth plate.
on the cranial aspect of the joint with the patella in the trochlear groove. When the patella is displaced medially,
the strength and tone of the quadriceps is lost. The lateral joint structures are stretched and the
medial structures contract.
TREATMENT AND PROGNOSIS
There are 4 significant modes of inheritance in dogs. These are autosomal (simple) recessive, autosomal dominant,
sex-linked recessive, and polygenic. Genes are the physical hereditary link between generations. Unless there are
mutations, inheritance is particulate, meaning that a given gene or set of genes is acquired by the progeny in an
all or none fashion. Each individual has 2 genes for each trait (simple Mendelian genetics). Each autosome
(non-sex chromosome) is present in duplicate since individuals receive one from each parent.
In addition to the autosomal or non-sex chromosomes, each animal has two sex chromosomes.
Dogs have thirty-nine pairs of chromosomes, thirty-eight are autosomal chromosomes and one pair of sex
Any organism is the product of its genes, or genotype, acting within
environment. Genetic traits cannot be caused by the environment, but modification of the expression can occur.
Simple Mendelian traits can be separated into dominant and recessive modes of inheritance. If the trait can
be expressed phenotypically by the sole presence of one gene of a gene pair, it is dominant. If both genes in
a pair are required to manifest the trait, it is said to be recessive. Not all traits are simple.
Some traits are controlled by a number of genes. Each of these genes adds in increments to the total phenotype.
These are called complex Mendelian traits. Because multiple genes are involved, distribution of specific phenotypes
cannot be predicted. The environment can make these traits more or less detrimental to the phenotype, but the dog
will only develop a disorder if it has the complement of genes necessary to produce that trait. Just as the environment
can modify polygenic traits, so can the genetic makeup of the individual. The expression of traits may vary as
a result of the total number of genes present, by the modification of normal structures, or by the modification
of the severity of the trait. Polygenic traits tend to show a continuous variation in the phenotype.
whole dog is composed of about 100,000 genes.
that cause the abnormal phenotype in the progeny. This contribution isn't necessarily equal between the
dam and sire. Since these traits are not sex-linked, there is an equal distribution of either sex affected.
trait may skip generations and may appear to be erratic in occurrence.
the canine genome contains 341 well-spaced markers that provide about 95% coverage. This means that
marker tests can and are being developed to help in strategic breeding plans to eliminate undesirable traits.
DNA tests for heritable disorders are the best method of evaluation because the genotype of the individual is
determined. Most of the current testing methods rely on phenotypic evaluation. The phenotype is the physical
expression of individual traits. The phenotype is the product of the environment and the genotype.
The phenotypic evaluation is less reliable than the genotypic (DNA) evaluation because carrier individuals
can be phenotypically normal.
Purebred dog breeders have been challenged by the problem of genetic disease for years. Goals must be established
to provide a direction. From a health prospective, breeding animals free from painful, disfiguring or lethal disorders
should be paramount. In order to breed these better dogs, breeders need information about the genetic propensities
of their dogs. Genetic databases must be the core to control of genetic disorders in our animals.
Control of heritable disorders is a complicated problem revolving around the provision of and use of information
the genetic composition of individuals.
To be of value for current breeding decisions, the information should not only be current and up-to-date
also encompass data on the entire family.
reveal the genotype of the individual. Studies have shown that selective breeding using phenotypic evaluations
can reduce the frequency of polygenically inherited disorders. There is no charge for entry of affected individuals
Both open and semi-closed databases will be available. The semi-closed database will make only normal results
to the public. The open database will list both normal and abnormal
individuals and pets. It will be necessary for breeders and prospective owners to be educated regarding the nature
of the disorder (method of inheritance) as well as the type of test (phenotypic versus genotypic)
used for the evaluation.
Patella luxation affects different breeds of dogs. Luxation is most commonly medial and can be bilateral.
It is considered to be a polygenically inherited disorder. The actual luxation is associated with multiple anatomical
abnormalities. The severity is categorized by 4 grades of luxation. Surgical procedures are available to provide for
a normalization of the physical aberrations. Surgical correction has been shown to produce good clinical results.
Selective breeding of phenotypically normal individuals should be utilized to decrease the frequency of the disorder.