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Review Article
A review of osteoarthritis and
obesity: current understanding
of the relationship and benefit
of obesity treatment and prevention
in the dog
W. G. Marshall1; B. A. Bockstahler2; D. A. Hulse3; S. Carmichael1
1Small Animal Hospital, University of Glasgow Veterinary School, Glasgow, Scotland; 2Clinical Department of Small
Animals and Horses, University of Veterinary Medicine, Vienna, Austria; 3The Department of Small Animal Medicine
and Surgery, College of Veterinary Medicine, Texas A & M University, College Station, Texas, USA
Keywords
Obesity, osteoarthritis, canine, human
Summary
Obesity is an increasingly important health
problem for both man and dog. Osteoarthritis
(OA) is a significant cause of pain and disabil-
ity in both species. A link between obesity and
OA has been established in man, though the
exact mechanism of the relationship remains
to be fully elucidated – current research sup-
ports both biomechanical and biochemical
theories. There is good evidence (class I*) to
support weight loss as an effective treatment
for human knee OA. In the dog, the relation-
ship is just beginning to be investigated. The
results of one study in dogs (class IV evi-
dence*) suggest that preventing the develop-
Vet Comp Orthop Traumatol 2009; 22: 339–345
doi:10.3415/VCOT-08-08-0069
Received: August 2, 2008
Accepted: February 23, 2009
Prepublished online: August 28, 2009
Correspondence to
William G. Marshall, BVMS
Small Animal Hospital
University of Glasgow Veterinary School
Bearsden Road
Glasgow, Scotland G61 1QH
UK
ment of overweightness and obesity reduces
the prevalence of hip dysplasia and OA of the
hip and other joints. Three other studies (class
III and IV evidence*) support weight loss as an
effective treatment for OA in affected over-
weight and obese dogs. Further research
could yield greater understanding of the pa-
thophysiology of this relationship, perhaps
identifying novel therapeutic targets. Confir-
mation and better understanding of the posi-
tive effect of treating and preventing obesity
on symptoms and prevalence of OA is likely to
be valuable in the campaign against canine
obesity.
* Classes of evidence detailed in Table 1.
339 © Schattauer 2009
Vet Comp Orthop Traumatol 5/2009
Introduction
The World Health Organisation has declared
obesity to be the most important health prob-
lem currently facing the Western world (1). In
humans, body mass index (BMI) is calculated
using the formula; body mass (kg) / height
(m)
2
, and obesity and overweightness are de-
fined as a BMI = 30 and = 25 respectively (2) .
In the United States in 2004, 33% of adults
were considered obese and 17% of teenagers
overweight (2). A study published in 1986 es-
timated the prevalence of canine obesity to be
24% and a similar study published in 2005
gave a figure of 41% (3, 4). It is widely sus-
pected among veterinarians that the preva-
lence of obesity among populations of do-
mestic dogs is increasing. Currently obesity
and overweightness in the dog are arbitrarily
defined as relative bodyweight = 120% and =
110% respectively (5). Relative bodyweight is
calculated by dividing actual weight by an es-
timated ideal body weight and multiplying by
100%. Osteoarthritis (OA) is the most com-
mon cause of pain and physical disability in
man, and is likely to be of similar significance
in the dog, with an estimated 20% of adult
dogs affected (6, 7). Obesity has consistently
been identified as a risk factor for the devel-
opment of OA in man, with the strongest evi-
dence supporting a relationship with knee
OA. It is now recognised that reducing the
prevalence of OA and its associated burden
on health services requires a commitment to
tackling the obesity pandemic (8).
Aim of review
The purpose of this review is to summarise
current theories surrounding the relationship
between obesity and OA in man, and to sys-
tematically review the literature pertaining to
a similar relationship in the dog. Two ques-
tions are raised in the systematic review:
first – does prevention of canine overweight-
ness and obesity reduce OA prevalence, and
second – will weight loss alleviate clinical
signs of pain and disability in overweight and
obese dogs with OA?
Obesity and osteoarthritis
in man
Obesity has consistently been identified as a
risk factor for development of knee and hand
OA, and for the progression of knee OA
(9–11). The relationship between obesity and
hip OA is not so convincing: a meta-analysis
performed in 2002 found only moderate evi-
dence to support it, and two recent studies did
not find any association (9, 10, 12). The
mechanisms by which obesity can affect the
development and progression of OA (in those
joints where a relationship has been estab-
lished) is the subject of a significant volume
of current research in human rheumatology.
Obesity, joint biomechanics
and osteoarthritis
Joint loading is essential for the maintenance
of healthy cartilage, but a reduction or an in-
crease in loading outside normal physiologic
levels, or a change in the direction of joint
forces (e.g. with joint instability) can be detri-
mental (13). Current understanding of knee
OA in man suggests that initiation of the dis-
ease requires not only an increase in load, but
also that joint kinematics are altered so that
weight-bearing is shifted to areas of cartilage
incapable of sustaining such loads (13). Joint
kinematics may be altered by some primary
abnormality of congruity or stability, or by a
load-bearing shift secondary to excess body-
weight itself. By altering joint kinematics and
increasing ambulatory load, obesity may have
roles both in the initiation and progression of
OA (14).
Illustrating the importance of joint kine-
matics are two studies that examined the in-
fluence of knee alignment. The first study
demonstrated that there was a significant re-
lationship between BMI and radiographic se-
verity of OA in human knees with a varus, but
not valgus alignment (15). The authors sug-
gested that the increased axial load on articu-
lar cartilage is concentrated across the medial
joint compartment by varus malalignment,
and that such malalignment, combined with
a long moment arm with respect to the centre
of gravity at the knee, may explain the strong
link between obesity and knee OA (15). The
second study found that the progression of
knee OA was positively associated with in-
creasing BMI, but only where moderate mala-
lignment (valgus or varus) was present (16).
Again the theory is that malalignment acts to
concentrate the increased joint forces caused
by obesity thus precipitating cartilage dam-
age.
The biomechanical aspect of any relation-
ship between obesity and OA is far from being
completely understood. However, there is
considerable evidence to suggest that the link
between knee OA and obesity is, at least in
part, a biomechanical one and that malalign-
ment may be an important mediating factor
(15, 16).
Obesity, adipokines and
osteoarthritis
Obese people are at increased risk for devel-
oping OA of certain joints of the hand. As
these joints are non weight-bearing, this sug-
gests a metabolic rather than mechanical as-
sociation between obesity and OA (11). Adi-
pose tissue can no longer be considered a
simple energy reserve – it has many functions
beyond the storage of triglyceride and release
of fatty acids. The adipocyte is capable of syn-
thesising and releasing a variety of molecules
with immunological or endocrine function
including the ‘adipokines’ leptin and adipo-
nectin. Indeed, it has been proposed that adi-
pose tissue should be thought of as an organ
in its own right (17).
Leptin is a peptide hormone, produced by
the adipocyte, which has received much at-
tention in attempts to understand the rela-
tionship between obesity and OA. It plays a
major role in regulating appetite through ac-
tivation of hypothalamic receptors, but also
participates in various other biological pro-
cesses – inflammation and immune function
in particular (18). There is a growing body of
evidence to suggest that leptin has a detri-
mental effect on articular cartilage, and a role
in the pathogenesis of OA (19). A key paper
on leptin was published recently by Simopou-
lou and colleagues who hypothesised that OA
is a metabolic disease caused by systemic and
local factors including altered lipid metab-
olism (20). They demonstrated that in people
with OA of the knee or hip, leptin levels were
significantly elevated in synovial fluid com-
pared to serum and that chondrocytes cul-
tured from healthy or arthritic cartilage could
express leptin mRNA and protein. Expression
of leptin and Ob-Rb (leptin receptor) mRNA
was significantly increased in chondrocytes
cultured from cartilage affected by OA com-
pared to normal tissue, and in advanced OA
compared to minimally affected cartilage. In
severely affected cartilage, leptin mRNA ex-
pression was significantly increased in obese
compared to normal weight patients, suggest-
ing a local as well as systemic hyperleptinae-
mia in these individuals. Leptin has an in-
hibitory effect on the long-term growth of
cultured chondrocytes, and induces the pro-
duction of interleukin-1 (IL-1), matrix
metalloproteinase-13 (MMP-13) and
MMP-9 in a dose-dependent manner, which
signifies a catabolic effect on chondrocyte
metabolism (20).
The biochemical relationship between
adipose tissue and arthritis is unlikely to be
mediated by leptin alone. Adiponectin is an-
other cytokine synthesised and released by
fat, and by other tissues. It is present within
the systemic circulation and is also produced
by local joint tissues such as the adipocytes of
the infrapatellar fat pad and synovial fibrob-
lasts (17). Treatment of synovial fibroblasts
from joints affected by OA with adiponectin
in vitro induces production of pro-MMP-1
and IL-6 which play key roles in cartilage des-
truction (17).
It was recently demonstrated that human
and murine chondrocytes express functional
adiponectin receptors, and that treatment of
these cells with adiponectin induces ex-
pression of nitric oxide synthase type II
(NOS2), IL-6, MMP-3, MMP-9 and mono-
cyte chemoattractant protein-1 (MCP-1). Ni-
tric oxide (NO) (produced by NOS2) con-
trols cartilage functions including loss of
chondrocyte phenotype, chondrocyte apop-
tosis and extracellular matrix degradation.
Interleukin-6, MMP-3, MMP-9 and MCP-1
are all mediators of cartilage degeneration
(21). An understanding of the role of adipo-
kines in OA pathophysiology is important as
they may represent target molecules for novel
therapeutic compounds.
Other obesity related
diseases and osteoarthritis
Cardiovascular disease appears to have an as-
sociation with both obesity and OA. It has
been proposed that atherosclerosis of sub-
chondral bone microvasculature and result-
ing bone ischaemia may contribute to the
progression of OA (22). This raises the ques-
tion of whether treatment of hypercholeste-
rolaemia could help to slow the progression
of the disease (22).
An association between diabetes and hand
OA has been demonstrated and one theory to
explain this association focuses on advanced
W. G. Marshall et al.: A review of osteoarthritis and obesity 340
Vet Comp Orthop Traumatol 5/2009 © Schattauer 2009
341 W. G. Marshall et al.: A review of osteoarthritis and obesity
© Schattauer 2009 Vet Comp Orthop Traumatol 5/2009
glycation end products (AGE), which form
within many tissues as part of the ageing pro-
cess (23). The deposition of these products is
accelerated by diabetes mellitus, including
obesity-induced type 2 diabetes (23). The
AGE accumulate in articular cartilage and
may have several detrimental effects on that
tissue; cross-linking of AGE causes increased
stiffness of collagen and compromises the
mechanical properties of cartilage (23).
Chondrocytes express a receptor for AGE,
stimulation of which results in activation of
inflammatory pathways and MMP-13 pro-
duction (24). The AGE increase matrix
degradation and decrease proteoglycan syn-
thesis (25). If AGE play a role in OA patho-
genesis, then prevention and treatment of
type 2 diabetes could indirectly reduce OA
prevalence. In addition, administration of
compounds such as pyridoxamine that in-
hibit AGE formation could represent a novel
therapy for OA (23).
An understanding of the complex rela-
tionship between obesity and OA is slowly
evolving. It is conceivable that from any one
of the four potential contributing factors dis-
cussed here (biomechanics, adipokines, vas-
cular disease, and diabetes), novel therapies
for treating OA might be developed that
would actually modify the disease process.
Some of these treatments could be of benefit
to canine as well as human patients, but only
if we further develop our understanding of
this relationship in the dog.
Benefit of weight loss in
human osteoarthritis
Although the pathogenesis and relationship
of obesity and OA may require further eluci-
dation, and may yield valuable pharmaco-
logic therapies in the future, the evidence to
support weight loss itself as a therapeutic in-
tervention for obese people with OA is dif-
ficult to dispute – at least in the case of knee
OA. A recent meta-analysis showed that a
5.1% reduction in bodyweight within a 20
week period could significantly reduce self-
reported disability in obese patients with OA
of the knee (26). Similar studies examining
the effect of weight loss on symptomatic hand
OA do not yet exist within the literature, to
the authors’ knowledge.
Obesity and osteoarthritis
in dogs
Investigative method
By searching the Medline database from 1950
to 2008 via PubMed using the following
search terms; ‘dog and obesity and osteoar-
thritis’, ‘dog and weight loss and osteoarthri-
tis’ and ‘dog and dietary restriction’, papers or
abstracts were identified that described either
the effect of becoming overweight or obese
on the development and progression of OA,
or the effect of weight loss on clinical signs of
OA in overweight or obese dogs. Any suitable
publications known to the authors but not re-
vealed by the database search were also in-
cluded. The identified studies were classified
based on their quality according to a scheme
proposed for examination of evidence in vet-
erinary orthopaedic surgery (27, 28) (
!
Table
1). Eleven prospective studies were identified
that described treatment or prevention of
overweightness and obesity in dogs and the
associated effect on OA (
!
Table 2).
Effect of preventing
overweightness and obesity on
the development of osteoarthritis
in the dog
The papers reviewed in this section (29–36)
are the result of an experimental study that
examined the effect of food restriction in La-
brador Retrievers that were genotypically
predisposed to hip dysplasia. Forty-eight
dogs from seven litters of experimental ani-
mals were paired by sex and bodyweight and
randomly divided into ‘control-fed’ and
‘limit-fed’ groups of twenty-four. The control
group was initially fed ad libitum, and then at
around three-years-old their intake was re-
duced to 62.1 kcal of metabolisable energy
per kilogram of ideal bodyweight per day. The
limit-fed group was given 75% of the food
consumed by the control group. The magni-
tude and rate of bodyweight gain were signifi-
cantly less in the limit group over the first two
years of life. Mean body-condition scores at
12-years-old were 4.6 and 6.7 out of nine for
limit-fed and control dogs respectively. The
Table 1 Levels of evidence. Modified from Aragon and Budsberg (2005) and reproduced from Innes
(2007) (27, 28).
Evidence
class
Study design Examples, comments
I Evidence derived from multiple,
randomised, blinded, and
placebo-controlled trials in the
target species.
Systematic reviews (e.g. meta-analyses).
Advantages of meta-analyses include:
●objective appraisal,
●large number of subjects,
●improved estimates of association,
●assimilation of large quantities of information,
●findings developed on a common scale, and
●improved quality of primary research.
II Evidence derived from high
quality clinical trials using
historical controls.
Randomised-controlled clinical studies.
Studies that are done on animals that developed
the disease naturally and are performed in the
laboratory setting. Historical controls are thought
to be less reliable than randomised controls.
III Evidence derived from
uncontrolled case series.
Non-randomised, prospective case
comparison studies.
Examples include prospective case series that in-
clude subjective clinical impressions to objective
gait analysis.
IV Evidence derived from expert
opinion, or are extrapolated from
research or physiological studies.
Retrospective case comparison studies.
Studies on research subjects (non-client owned)
are also included in this class.
dogs were examined at intervals throughout
their lifetime for evidence of disease. Because
experimental animals were used, this study
can be considered class IV evidence, but the
use of client-owned animals would have been
extremely difficult and may have precluded
the use of a randomised, controlled design.
On average, the control dogs became over-
weight and the limit-fed dogs maintained a
body condition score very close to normal;
this study compared the overfed (control-
fed) and optimally-fed (limit-fed) dogs.
Radiographic examination of the hip
joints was performed when the dogs were 30,
42, 54, 78 and 104-weeks-old. Measurement
of the Norberg angle on a standard (hips ex-
tended) radiograph of the pelvis at 30-weeks-
old revealed significantly less dysplasia
among the limit-fed dogs. Norberg angles
were measured again when the dogs were
two-years-old; hip dysplasia scoring was also
performed at this time using both the Ortho-
pedic Foundation for Animals and Swedish
Kennel Club systems. At two-years–old, 16 of
the 24 control dogs and seven of the 24 limit-
fed dogs showed radiographic evidence of hip
dysplasia. The reason why limiting food in-
take reduced the incidence of hip dysplasia is
unknown, and may not be the result of de-
creased bodyweight alone, but could also be a
consequence of decreased growth rate. With-
out a complete understanding of the mech-
anism, it can still be said that dietary restric-
tion appears to be an environmental change
that can improve the phenotype of animals
genotypically predisposed to hip dysplasia.
The authors of this study recognised poten-
tial concerns, in that this approach may per-
petuate hip dysplasia in the canine popu-
lation; however they felt that efforts to reduce
the incidence of dysplasia were justifiable and
required. This study highlights the need for a
canine hip dysplasia test that is not influenced
by environmental factors (29).
Pelvic radiographs were repeated when
the dogs were three- and five-years-old. These
and all previous images were examined for
evidence of OA. At the age of one year, there
was a significant difference in the frequency
and severity of coxofemoral OA between the
two groups of dogs: sclerosis of the cranio-
dorsal portion of the acetabulum was present
in seven of the control-fed and none of the
limit-fed dogs. At two-years-old, 10 of the 24
control dogs showed radiographic evidence
of hip OA compared with one of the 24 limit-
fed dogs. By the age of three-years, 12 of the
23 control dogs showed OA versus three of
the 23 limit-fed dogs (1 dog from each group
had died by this time). The number of dogs
affected by hip OA in each group did not
change between the ages of three and five,
though the radiographic severity did increase
in both groups. Bodyweight among the limit-
fed group was 25% less than the control-fed
group, and it was significantly correlated with
the severity of OA. On the basis of their re-
sults, the authors recommend that dogs be
maintained in ‘slender’ body condition
throughout their period of growth and adult
lives to reduce the incidence of hip OA (30).
At eight-years-old, 15 of the 22 control-fed
and three of the 21 limit-fed dogs had radio-
graphic hip OA, with greater severity in the
control group (both of these findings were
statistically significant). Bilateral hip OA was
more common than unilateral in a ratio of 2:1
(31).
In 2006, another paper was published on
the development of hip OA in the same dogs
(23). Confusingly, prevalence of hip OA
seemed to have decreased among the control
dogs from when these results were first re-
ported. This discrepancy is probably because
only one investigator interpreted the radio-
graphs, whereas the median OA score of three
investigators’ interpretation had previously
been reported . When the dogs died (end of
life – EOL) 20 of the 24 control-fed and 12 of
the 24 limit-fed dogs had radiographic hip
OA. The hip joints were not examined at
postmortem.
!
Table 3 illustrates the devel-
opment of hip OA in the two groups of dogs
during their lifetime.
Radiographic examination of the elbow,
stifle and shoulder joints was performed
when the dogs were eight-years-old; the
prevalence of OA affecting multiple joints
was significantly greater in the control group.
Ten of the 22 control dogs had OA in two dif-
ferent joints versus one of the 21 limit-fed
dogs. Eight of the 22 control dogs and four of
the 21 limit-fed dogs had elbow OA; this dif-
ference was not significant, however the
radiographic OA severity was greater in the
control group. At EOL, elbow OA was more
prevalent when assessed radiographically,
Vet Comp Orthop Traumatol 5/2009 © Schattauer 2009
342 W. G. Marshall et al.: A review of osteoarthritis and obesity
Table 2 Studies that have examined the effect of treatment or prevention of overweightness and
obesity on osteoarthritis in dogs.
Reference
number
Method: treatment
or prevention?
Co-morbidity examined Evidence
class
29 Prevention Hip dysplasia IV
30 Prevention Radiographical signs of hip osteoarthritis IV
31 Prevention Radiographical signs of osteoarthritis in
multiple joints
IV
32 Prevention Radiographical signs of hip osteoarthritis IV
33* Prevention Radiographical and pathological evidence of
elbow osteoarthritis
IV
34 Prevention Radiographical and pathological evidence of
shoulder osteoarthritis
IV
35 Prevention Various diseases including osteoarthritis;
lifespan
IV
39 Treatment Clinical signs of osteoarthritis (various joints,
subjective and objective outcome measures)
III
* Abstract in proceedings.
36 Prevention Lifespan and causes of death IV
37* Treatment Clinical signs of hip osteoarthritis
(objective outcome measure)
IV
38 Treatment Clinical signs of hip osteoarthritis
(subjective outcome measure)
III
however there was no difference in prevalence
when the joints were examined postmortem.
An explanation for the difference in preva-
lence for radiographic and postmortem OA
of the elbow is not given, however it could be
due to over interpretation of the radiographs.
Histopathologic severity of elbow OA was
greater in the limit-fed dogs at EOL (33). Two
of the control dogs had radiographic stifle OA
at eight-years-old; none of the limit-fed dogs
did (31).
The most recently published paper by this
group focuses on shoulder OA (34). Radio-
graphic examination of the shoulder was per-
formed at six- and eight-years-old . Gross and
histopathological evaluations of the various
components of the shoulder joint were per-
formed at EOL. The radiographic and patho-
logical prevalence of shoulder OA in both
groups is illustrated in
!
Table 4.
Similar to elbow OA, severity but not
prevalence of shoulder OA was lower at the
ages of six- and eight-years in the limit-fed
dogs. There was not any difference in preva-
lence or severity at EOL; though it should be
noted that median lifespan among the limit-
fed dogs was 1.8 years longer. Ninety-one per-
cent of all dogs had histopathological evi-
dence of shoulder OA at EOL; this high over-
all prevalence of OA is striking. Radiographic
and pathological evidence of shoulder OA
were poorly correlated.
Overall, diet restriction reduced the preva-
lence and severity of OA, and had by far its
most significant effect on OA of the hip joint.
This was almost certainly a consequence of a
reduced prevalence of phenotypic hip dyspla-
sia in the limit-fed dogs. By comparison,
prevalence of shoulder OA was high in both
groups of dogs, but it was not significantly
different between them. Lesions consistent
with osteochondrosis were not found at post-
mortem, and for this reason the authors pro-
pose that the shoulder OA in this population
of dogs was primary in nature (34). If this is
the case then it can be suggested that the effect
of diet restriction on development of primary
OA (OA with no apparent predisposing fac-
tor) is not as significant as its effect on hip
joint laxity and subsequent (secondary) OA.
Osteoarthritis was the most common
chronic disease to develop in both groups.
The control dogs required institution of long-
term treatment for OA on average three years
earlier then the limit-fed dogs. This is the first
indication of the clinical significance of OA
diagnosed radiographically – it seems that the
control dogs displayed clinical signs earlier as
well, however lameness was not evaluated
either subjectively or objectively. It is interest-
ing to note that debilitating OA was a leading
cause of death (euthanasia) in both groups.
Seven limit-fed versus 11 control dogs were
euthanatized because of OA at mean ages of
11.5 and 13.1 years respectively. In general,
causes of death between the two groups of
dogs were similar; it was the time of death
that differed; with limit-fed dogs living (on
average) 1.8 years longer (35, 36).
In summary, from the series of pub-
lications resulting from this long-term study
(29 –36), it seems that maintaining Labradors
at a body condition score of around five out of
nine for life may:
●
reduce the incidence of hip dysplasia,
●
reduce the incidence or severity of OA
depending on the joint in question,
●
delay the need for treatment of OA (and of
other chronic diseases),
●
delay the need for euthanasia due to
chronic disease (OA was a leading cause of
euthanasia),
●
delay natural death due to disease other
than OA.
Benefit of weight loss in canine
osteoarthritis
Sixteen overweight and obese dogs with os-
teoarthritis (OA) of the hips showed im-
proved hindlimb function with a reduction of
body condition score: original scores of six to
eight improved to four to five based on a scale
of nine (37). The improvement was demon-
strated by comparison of kinetic gait analyses
at the beginning and end of weight loss: peak
ground reaction force increased and time of
the stride propulsive phase decreased. In-
creased peak vertical force (PFz) was ob-
served in both fore and hindlimbs and ranged
from 0.24 to 0.98 N/kg, with the greatest in-
crease being observed in the weakest hind-
limb. The decrease in time of the propulsive
phase of the stride ranged from 10.9 to 14.2
ms. The increase in PFz seen in the forelimbs
was interesting, but the greatest increase of
0.52N/kg seen in the strongest forelimb was
very modest (equivalent to 5% bodyweight).
© Schattauer 2009 Vet Comp Orthop Traumatol 5/2009
343 W. G. Marshall et al.: A review of osteoarthritis and obesity
Table 3
Prevalence of radio-
graphic hip osteo-
arthritis at selected
ages and at end-of-
life in limit-fed and
control dogs.
Dog group Limit-fed (%) Control-Fed (%)
Reference
number:
30, 31* 32 ** 30, 31* 32**
1-year-old 0 -- 29 --
2-years-old 4 4 42 25
5-years-old 13 13 52 39
8-years-old 14* 14 68* 64
End-of-life -- 50 -- 83
* Prevalence of hip osteoarthritis at eight-years-old in this column is derived
from reference 31.
** Reference 32 was published after reference 30 and 31 and gives differ-
ent values for prevalence of hip OA among the control population, possible
due to differences in the method of radiographic interpretation.
Table 4
Radiographic and
pathological preva-
lence of shoulder
osteoarthritis in
limit-fed and control
groups of Labradors.
Age (years) Examination
method
Limit-fed (%) Control-fed (%)
6 Radiographical 43 68
End-of-life Radiographical 83 74
Gross pathology 83 91
8 Radiographical 62 81
Even though it was statistically significant, it
may not be biologically significant. The de-
crease in time of the propulsive phase of the
stride suggests that the dog’s gait had changed
with an increased limb velocity, which may
suggest improved joint comfort.
This clinical trial demonstrated an objec-
tive improvement in lameness with weight
loss. It is difficult however to visualise the sig-
nificance of the reported changes in gait pa-
rameters without an accompanying descrip-
tion of clinical signs, subjective gait assess-
ment, or the owners’ perception of their dogs’
level of disability. Also, the data remains un-
published and can therefore only be consider-
ed, at best, class IV evidence.
Subjective outcome measures were uti-
lised by a different clinical trial that also
examined the effect of weight reduction on
lameness caused by OA, and represents class
III evidence (38). Nine dogs that were
11–12% greater than their estimated ideal
bodyweight and had clinical and radio-
graphic signs of hip OA completed the study.
A 40% reduction in caloric intake resulted in
weight loss of between 11 and 18% over a
period of 10 to 19 weeks. By the midpoint of
the weight loss period, mean bodyweight had
decreased significantly from 39.0 to 36.6 kg (a
6.2% decrease). This was accompanied by a
significant decrease in body condition score
and in subjective lameness score using nu-
merical rating and visual analogue scales. The
major limitation of this study was the oppo-
site to that of the previously mentioned work;
there was no objective confirmation of the
observed improvement in lameness.
The final study identified in this area was a
prospective clinical trial that did combine
subjective and objective outcome measures,
and also represents class III evidence (39).
Twenty-nine dogs with a body condition
score of four to five out of five were enrolled.
Selection criteria dictated that lameness was
observed in one limb only and that OA was
present in that limb. Dogs with OA of the hip,
elbow, stifle and shoulder were included. The
weight loss program was designed to produce
a one percent reduction in bodyweight per
week. Bodyweight, subjective lameness and
pain scores were evaluated monthly. Kinetic
gait analysis was performed bimonthly using
four force-plates mounted in a treadmill.
Asymmetrical weight distribution between
limbs affected and unaffected by OA was
demonstrated using symmetry indices, calcu-
lated for PFz and vertical impulse (IFz) by di-
viding greatest by least values for contralat-
eral limbs (e.g. sound limb divided by lame
limb). Weight loss was combined with
physiotherapy: dogs were randomly allocated
to an intense (group 1) or moderate (group 2)
physiotherapy program. Owners of dogs in
both groups were instructed to perform
massage, passive range of motion and to
gradually increase levels of controlled exer-
cise. Group 1 dogs were additionally treated
in a physiotherapy clinic twice weekly; this
treatment included application of transcut-
aneous electrical nerve stimulation.
A difference in weight loss was first de-
tected at day 90, and after six months group 1
had lost more weight than group 2 (13.6% of
initial body weight versus 9.3%). Lameness
scores decreased significantly, starting at day
30 in group 1 and at day 60 for group 2. Pain
scores also decreased, again the difference
reached significance sooner in group 1 (at 60
versus 90 days). The difference in lameness
scores between groups 1 and 2 was significant
only at days 30 and 180. There was not any
difference in pain scores between the two
groups. Symmetry indices for PFz and IFz in
group 1 were significantly improved (i.e.
closer to 1) at each re-evaluation. In group 2,
only the symmetry index for PFz improved,
and only at day 120. There was no difference
in weight loss between the two groups at day
60, however significant improvement in PFz
and IFz symmetry indices was observed for
group 1. This suggests that at day 60, the ob-
jective improvement in lameness shown in
group 1 may have been the result of intensive
physiotherapy rather than weight loss. A
comparison of indices between groups indi-
cated a greater degree of symmetry in group
1, but only for PFz. Overall, the dogs in group
1 appeared to show a more substantial im-
provement in lameness than those in group 2.
It is difficult to interpret this result because
two treatment variables were examined
simultaneously – degree of weight loss and
intensity of physiotherapy – and it was not
possible to separate their effects. It can be said
that a combination of the two treatments
would effectively reduce disability in dogs
with OA.
Conclusion
Current research suggests that in man, obes-
ity is a risk factor for the development of hand
OA, and both the development and progres-
sion of knee OA (9–11). There is good evi-
dence to support weight loss as an effective
treatment for knee OA (26). The exact mech-
anism of the relationship between obesity
and OA is not completely understood, but
likely involves both biomechanical and bio-
chemical factors (15–25).
At present, based on four studies that rep-
resent class III and IV evidence, we have a li-
mited comprehension of the links between
growth, developmental orthopaedic disease,
OA and obesity in the dog. The work of Kealy
and colleagues suggests that restricting ener-
gy consumption during growth may reduce
the incidence of hip dysplasia; however a re-
cent experimental study did not confirm this
relationship (29, 40). It is accepted that hip
OA in the dog is initiated by abnormal joint
kinematics, secondary to underlying laxity,
and that OA in other joints usually occurs sec-
ondary to some initiating process (e.g. osteo-
chondritis dissecans, cranial cruciate liga-
ment rupture) (41). Obesity may be an im-
portant factor in driving the progression of
OA by increasing the load factor of such ab-
normal joints; we do not know to what extent
obesity itself may alter canine joint biomech-
anics. It has been shown that obesity causes a
systemic hyperleptinaemia in the dog, but
leptin’s potential importance in the patho-
genesis of canine OA is at present unknown
(42). In order to devise improved treatment
and prevention strategies, a more complete
understanding should be sought, but at the
same time we must consider the existing evi-
dence, and make suggestions based on it.
It is generally acknowledged that the
prevalence of overweightness and obesity in
domestic dogs is increasing. It is the authors
impression that the problem of canine obes-
ity is not effectively dealt with by the majority
of veterinarians. The reasons for this prob-
ably include ignorance about the importance
of obesity, disinterest in its treatment, and a
reluctance to confront clients on the issue. In
addition, even those veterinarians that are
pro-active in treating and preventing obesity
will meet with resistance and non-com-
pliance from many pet owners. On a positive
note, there has been a recent move within the
344 W. G. Marshall et al.: A review of osteoarthritis and obesity
Vet Comp Orthop Traumatol 5/2009 © Schattauer 2009
veterinary profession to highlight the scale
and significance of obesity in companion ani-
mals (43). Evidence that demonstrates, to
both veterinarians and their clients, the
health benefits of obesity treatment and pre-
vention must surely be fundamental to any
such campaign. This review shows, when OA
as a disease is associated with obesity, that we
have a limited but growing body of support-
ive evidence for two recommendations;
maintaining dogs at a normal body condition
score throughout their lives can be recom-
mended to optimise synovial joint health,
and bodyweight reduction will alleviate clini-
cal signs of OA in obese and overweight dogs.
345 W. G. Marshall et al.: A review of osteoarthritis and obesity
© Schattauer 2009 Vet Comp Orthop Traumatol 5/2009
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