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Obesity is increasingly common in our companion animal population. Over the last 20 years, incidence rates in the literature have ranged from 20% to 40%, with the 2014 AAHA Weight Management Guidelines for Dogs stating that up to 59% of pets in the United States are overweight.1 Obesity is defined as excess body fat capable of complicating and/or exacerbating disease. Dogs are considered clinically obese when they exceed 15% of their ideal body weight. In conjunction with total body weight, body condition is also important to evaluate. On a scale of 1 to 9, with 5 being ideal, each incremental increase in body condition score (BCS) is equivalent to 10% to 15% of excess body weight. Whereas an individual animal may fall within reported weight parameters for age, sex, and breed, he or she may still be overconditioned based on BCS.

Development of osteoarthritis is a multifaceted process. Logically, increased body mass places increased stress on joints. A prevailing theory regarding the progression of osteoarthritis is that severity increases as the magnitude of stress is compounded, especially on abnormal joints. The dog has a myriad of orthopedic anomalies that result in abnormal joint configuration ranging from congenital laxity, as with hip dysplasia; developmental anomalies, as occur with dysplastic elbows; and degenerative injury, exemplified by cranial cruciate ligament rupture. 

Other potential inciting factors include adipokines. Fat is an inflammatory tissue, and in humans more than 100 active cytokines have been identified that can potentiate arthritic change in non‒weight-bearing joints. As an example, leptin is one of the most widely studied satiety chemicals, and when present in excess can have deleterious effects on articular cartilage. 

Osteoarthritis is estimated to affect 20% of dogs over 1 year of age and is a common cause of euthanasia in companion animals. The majority of dogs encountered in specialty surgical practice for various consequences of arthritis are obese. The pain and lameness attributable to arthritis can result in an animal becoming more sedentary and thus contribute to additional weight gain. It can also be very difficult to engage an owner on the importance of weight loss. Although the veterinary literature is lacking in well-controlled studies using client-owned animals, there is evidence that weight loss of as little as 6% body weight results in clinical improvement in lameness scores.2

Effects Of Weight Loss On Clinical Signs Of Osteoarthritis

A study by German in 2011 examined quality of life in client-owned dogs before and after weight loss.3 Fifty dogs were enrolled through participation in the Royal Canin Weight Management Clinic. These pets were confirmed overweight by dual energy x-ray absorption (DEXA), which preferentially differentiates fat from lean tissue. Of these 50 animals, 30 reached their target “ideal” weight and were further analyzed. On average, dogs lost 24% of their body weight (10‒43.5%). In the animals that completed the program, pain scores were statistically lower than baseline, and vitality scores were improved. Twenty-one of thirty owners felt that their dogs had an improved quality of life, while the remaining nine did not answer the question. As with humans, there appears to be a health-related quality of life improvement in conjunction with weight loss in dogs. Additional small studies confirmed that weight loss alone improved lameness in dogs. Impellizeri studied nine overweight dogs with radiographic changes consistent with hip dysplasia.4 Improvement in lameness scores was noted with an average 10% body weight loss. Two separate lameness scales were used, and improvement was noted on both; however, these studies lack an objective form of measuring improvement.

As with humans, there appears to be a health-related quality of life improvement in conjunction with weight loss in dogs.

Brady and colleagues showed that obesity alone influences the gait of dogs.5 Using force-plate analysis, obese dogs were shown to exert greater ground reaction forces than lean dogs (approximately 25% greater), proportional to their body mass. Obese dogs also had a shorter swing phase of their gait in both the fore and hindlimbs (~8%). Dogs enrolled in this study had no known history of orthopedic injury, joint disease, or lameness on examination.  There was also a greater range of motion (ROM) in the joints of overweight dogs, in contrast to findings in obese humans, in whom joint ROM (especially in the knee) is decreased. The authors hypothesized that this increased ROM may represent an underlying failure in muscular strength. Lack of sufficient muscle to protect the joint from the weight of ambulation can lead to increased stress within the joint, which would be compounded if the joint were abnormal.

Studies using force-plate gait analysis have since objectively showed that weight loss alone is capable of improving lameness. Marshall studied a heterogeneous population of 14 obese client-owned dogs.6 Their body weight was at least 20% greater than ideal, and the dogs had radiographic evidence of osteoarthritis, often in multiple joints. Over the course of 16 weeks, they lost an average of 8.5% of their body weight, and 82% of the dogs showed improvement in lameness scores, with as little as 6% to 8% body weight decrease sufficient to effect a change. In cases of forelimb lameness, there was a typical disparity between the more severely affected limb and the more sound limb. Differences in peak vertical force and vertical impulse between the forelimbs reduced by 50% by the middle of the study and 80% by the end. 

Mlacnik has demonstrated the combined benefit of physiotherapy with weight loss.7 Twenty-nine client-owned dogs were recruited; they had a BCS of 4 or 5 on a 5-point scale and radiographic evidence of osteoarthritis. Dogs were separated into two groups, one that received at-home therapy and the other intensive, in-clinic physiotherapy. Goal weight for the 6-month study was set at 85% of starting weight. While weight loss was achieved in all dogs, intense therapy resulted in more rapid weight loss and quicker improvement in ground reaction forces when compared with the control group. The magnitude of weight loss was also enhanced with intense therapy (13.6% versus 9.3% weight loss). In the intense therapy group, 86% of the dogs achieved an ideal BCS of 3 by the end of the 6-month study period, compared with 53% of the group monitored at home.  

Wucherer and Conzemius expanded this concept to study obese dogs with cranial cruciate ligament (CCL) deficiency.8 Although nonsurgical treatment for CCL rupture in overweight dogs may not be ideal, active physiotherapy and weight loss can yield improved outcomes, with up to 63% of dogs achieving good clinical use of the affected limb by 52 weeks after injury. In this study, 10% weight loss was achieved in 16 weeks.

Effects Of Weight On Development & Progression Of Osteoarthritis

The studies described above show that weight loss reduces clinical signs of osteoarthritis: Pain scores drop as weight is lost, improvement is noted on lameness scales, and positive strides are made in objective measurements of limb use. These studies examine obese dogs that are placed on a weight management plan. The osteoarthritic changes are present at the onset of the study and are not examined further throughout the course of examination. 

Weight loss reduces clinical signs of osteoarthritis: Pain scores drop as weight is lost, improvement is noted on lameness scales, and positive strides are made in objective measurements of limb use.

Perhaps the most complete collection of data composed thus far in the veterinary literature regarding the effect of weight on the development and progression of osteoarthritis is that of the limit-fed Labrador retrievers used by the Purina Study group from 1987 to 2001. An experimental population of 48 Labrador retriever puppies was assembled at 6 weeks of age.  They represented seven litters of puppies that were genetically predisposed to development of hip dysplasia.  The puppies were paired into age- and sex-matched groups at 6 weeks of age.  At 8 weeks, one member of the pair was fed ad libitum, whereas the second member of the pair was fed 75% of the caloric intake of the control puppy. These two groups of dogs were fed via this plan until 3.25 years of age. At that time, they were transitioned from a growth-type diet to a maintenance diet. To prevent marked obesity, the control group was now fed an equivalent of 62.1 kcal of metabolizable energy per kilogram of body weight. Again, the matched pairs were restricted to 75% baseline caloric intake. Multiple radiographic studies of these animals, which were eventually committed to a lifelong study, were performed. Each dog underwent DEXA scanning once yearly from 6 years of age until death. All dogs received a complete necropsy at the time of death.

Kealy and Lawler published data from these dogs that proved calorie restriction had a positive correlation with life span.9 Forty-six of the 48 study dogs were eventually euthanized for humane reasons. Median life span was significantly decreased in the control group (11.2 years) versus the restricted-fed dogs (13 years). Mean body weight was significantly less in the restricted-fed group (26% on average) with a BCS of 4.6 versus 6.7 on the 9-point scale. Body fat percentage was consistently higher in the control group. Some form of radiographic osteoarthritis developed in 43 of the 48 dogs; 35 dogs eventually required treatment, 19 in the control group and 16 in the limited-fed group. The mean age to which 50% of dogs required continual treatment for osteoarthritis was significantly lower in the control group (10.3 years in the control group vs 13.3 years in the restricted-feeding group).

As these dogs aged, osteoarthritis was the most common chronic disease that developed in the population. Twenty-six dogs were eventually euthanized due to musculoskeletal disease, at an average of 10.6 years in the control group versus 13.1 years in the limited-fed group. Restricted feeding was demonstrated to result in a lower hazard of death from a musculoskeletal cause. Serial DEXA scans showed that a high percentage of lean body mass was protective against death, whereas increasing percentage of body fat mass was predictive of death.

Smith and colleagues examined radiographic evidence of hip osteoarthritis in this same group of Labrador dogs.10,11 Overall, 15% of dogs had radiographic evidence of arthritis at 2 years, which increased to 67% at 14 years. The incidence of arthritic change increased linearly in both groups; however, the age at first documentation of radio graphic arthritis averaged 6 years in the control group and 12 years in the calorie-restricted group. Similarly, the calorie-restricted group had less radiographic evidence of hip osteoarthritis at the 2-, 5-, and 8-year time points. This study was performed using the typical extended ventrodorsal pelvic films as required by the Orthopedic Foundation for Animals (OFA). At all ages examined, the control group had a higher percentage of radiographic arthritic change: 39% versus 13% in the restricted group at 5 years; 83% versus 50% at 12 years. 

This study proved that hip phenotype can change markedly in middle and late age, which was not previously accepted. A collateral benefit of the study was to demonstrate the superiority of the Penn-HIP method over traditional OFA radiography. When distraction indices were measured in this population as a measure of hip joint laxity, all of the dogs were found to be susceptible in this group, although according to OFA standards, only 42% to 51% of the pups were expected to develop dysplastic change. Upon necropsy at end of life, 98% had radiographic or histopathologic changes consistent with osteoarthritis/dysplasia. Using OFA criteria with ventrodorsal views taken at 2 years of age, 51% of control-fed dogs had hip osteoarthrtis compared with only 21% of the restricted-fed dogs. With the abnormal distraction indices measured on all animals, as well as the 98% incidence of arthritis at death, the OFA method was found to be influenced by body condition and not at all reliable in predicting development of arthritis over time.

The incidence of shoulder arthritis was high in this group, although no overt congenital cause was determined. Runge and others published data from the shoulders of these dogs evaluated at 6 years, 8 years, and end of life.12 There was great disparity demonstrated between radiologic changes and histopathologic evidence, which is a known difficulty of correlating radiographic change with clinical signs of lameness. 

While the frequency and distribution of gross shoulder lesions were similar between groups at necropsy, radiographic evidence of shoulder arthritis was demonstrated earlier in the control group than the limit-fed group. Sixty-eight percent of control-fed dogs had radiographic changes consistent with osteoarthritis at 6 years compared with 43% of the limit-fed group. Radiographic severity also was significantly less in the restricted-fed group at ages 6 and 8. 

The primary accomplishments of this facet of the study were to demonstrate the high prevalence of osteoarthritis in multiple joints in this group of dogs, as well as to suggest that this particular manifestation may be consistent with primary disease—arthritis due to age and wear—rather than abnormal conformation. The study also confirmed the low sensitivity of radiography in demonstrating arthritic change. Although gross and histopathologic changes in the joints of all dogs were similar by end of life, it is worth remembering that the joints of limit-fed dogs were on average 1.8 years older than those of the control group.  

Similar results were demonstrated when the elbow joints were examined.13 Unfortunately, initial radiographic assessment was not attempted until 6 years of age. Again, radiographic severity was increased in the control group, but histologic changes at end of life were similar. Histologically, the joints lacked the classic hallmark changes of elbow dysplasia (joint incongruency, fragmented medial coronoid process, ununited anconeal process), although a high proportion had an ununited medial epicondyle, which is thought to be very rare. Despite the evidence of histopathologic arthritis in 60% to 65% of dogs in this study, only two dogs in the restricted calorie group and five in the ad-libitum control group developed lameness consistent with elbow arthritis.

There is a great deal of translational research still to be performed to thoroughly investigate the link between obesity and osteoarthritis in the dog. The Labrador retriever study group provides invaluable data proving that dogs at a lean body condition live up to 2 years longer than those that are overweight. As many of the animals in this study were euthanized for musculoskeletal reasons, it can be stated that increased body weight has a detrimental effect on joint health. As the overweight and obese dogs in this population had an average body condition score of 6.7 on a 9-point scale, it stands to reason that the morbidly obese canine population may have even poorer statistics when joint comfort is considered. While large studies are lacking, there is good evidence, both subjective and objective, that relatively small changes in body weight can increase comfort level in obese, arthritic dogs.

References Show
References
  1. Brooks D, Churchill J, Fein K, et al. 2014 AAHA weight management guidelines for dogs and cats. J Am Anim Hosp 2014;50:1-11.

  2. Marshall WG, Hazewinkel HAW, Mullen D, et al.  The effect of weight loss on lameness in obese dogs with osteoarthritis.  Vet Res Commun 2010;34:241-253.

  3. German AJ, Holden SL, Wiseman-Orr ML, et al.  Quality of life is reduced in obese dogs but improves after successful weight loss.Vet J 2012;192:428-434.

  4. Impellizeri JA, Tetrick MA, and Muir P.  Effect of weight reduction on clinical signs of lameness in dogs with hip osteoarthritis.  J Am Vet Med Assoc 2000;216:1089-1091.

  5. Brady RB, Sidiropoulos AN, Bennett HJ, et al.  Evaluation of gait-related variables in lean and obese dogs at a trot.  Am J Vet Res 2013;74:757-762.

  6. Marshall WG, Bockstahler BA, Hulse DA, et al.  A review of osteoarthritis and obesity: current understanding of the relationship and benefit of obesity treatment and prevention in the dog. Vet Comp Orthopaed 2009;22:339-345.

  7. Mlacnik E, Bockstahler BA, Müller M, et al.  Effects of caloric restriction and a moderate or intense physiotherapy program for treatment of lameness in overweight dogs with osteoarthritis.  J Am Vet Med Assoc 2006;229:1756-1760.

  8. Wucherer KL, and Conzemius MG.  Short-term and long-term outcomes for overweight dogs with cranial cruciate ligament rupture treated surgically or nonsurgically.  J Am Vet Med Assoc 2013;242:1364-1372.

  9. Kealy RD, Lawler DF, Ballam JM, et al.  Effects of diet restriction on life span and age-related changes in dogs.  J Am Vet Med Assoc 2002;220:1315-1320.

  10. Smith GK, Pastor ER, Powers MY, et al.  Lifelong diet restriction and radiographic evidence of osteoarthritis of the hip joint in dogs.  J Am Vet Med Assoc 2006;229:690-693.

  11. Smith GK, Lawler DF, Biery DN, et al.  Chronology of hip dysplasia development in a cohort of 48 Labrador Retrievers followed for life.  Vet Surg 2012;41:20-33.

  12. Runge JJ, Biery DN, Lawler DF, et al.  The effects of lifetime food restriction on the development of osteoarthritis in the canine shoulder.  Vet Surg 2008;37:102-107.

  13. Huck JL, Biery DN, Lawler DF, et al.  A longitudinal study of the influence of lifetime food restriction on development of osteoarthritis in the canine elbow.  Vet Surg 2009;38:192-198.  

Suggested Reading 

  • Laflamme DP.  Obesity in dogs and cats: What is wrong with being fat? J Anim Sci 2012;90:1653-1662.
  • Lawler DF, Evans RH, Larson BT, et al.  Influence of lifetime food restriction on causes, time, and predictors of death in dogs.  J Am Vet Med Assoc 2005;226:225-231.

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