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Can Vet J. 2010 March; 51(3): 289–292.
PMCID: PMC2822373

Language: English | French

Kinematic characteristics of myositis ossificans of the semimembranosus muscle in a dog


A 6-year-old Doberman pinscher dog was presented with myositis ossificans of the semimembranosus muscle. Linear, temporal, and angular kinematic patterns were recorded and compared with those of sound dogs of the same breed. The results indicate that the specific gait compensations occurring with this disease may aid in the diagnosis of myositis ossificans of the caudal thigh muscles.


Caractéristiques cinématiques de la myosite ossifiante du muscle semi-membraneux chez un chien. Un chien Doberman pinscher âgé de 6 ans a été présenté avec une myosite ossifiante du muscle semi-membraneux. Des modèles cinématiques linéaires, temporels et angulaires ont été enregistrés et comparés à ceux de chiens de la même race en santé. Les résultats ont indiqué que les compensations spécifiques de la démarche se produisant avec cette maladie peuvent aider au diagnostic de myosite ossifiante des muscles inférieurs des hanches.

(Traduit par Isabelle Vallières)

“Myositis ossificans” or “ossifying myopathy” is a benign condition caused by heterotopic non-neoplastic bone formation due to metaplastic evolution of a fibrotic contracture or myopathy (1). The condition, described mainly in horses (1,2) and dogs (3,4), generally affects the caudal muscles of the thighs as well as the biceps, semitendinosus, semimembranosus, gracilis, and sartorius muscles (5). The most widely accepted etiology is trauma that arises from either intense exercise or intramuscular injections. Pathology evolves with a gradual replacement of the muscle fibers by fibrous tissue and the production of irregular jagged plaques of spongy bone in the interstices (6). The prevalence of myositis ossificans in dogs is very low. Doberman pinschers with von Willebrand’s factor deficiency were over-represented in early reviews, but more recent reports have described the condition in other breeds of dog (7).

The clinical diagnosis of myositis ossificans has traditionally been made by observation of a characteristic alteration of gait, where an animal will walk with a “goose step” or “jerky gait,” as well as a characteristic fibrotic or ossified muscle mass identified by palpation of the limb (5).

Kinematic gait analysis in dogs is progressively being included as a tool in the objective quantification of both normal gait and specific disorders that induce lameness in dogs (811). This case report quantifies the gait compensation observed in a case of myositis ossificans of the semimembranosus muscle in a dog.

Case description

A 6-year-old Doberman pinscher used for intense agility work was referred to the Veterinary Hospital of the University of Las Palmas de Gran Canaria with a 6-month history of pro-gressive lameness of the left pelvic limb. On clinical examination, a lateral depression in the distal part of the thigh could be observed (Figure 1a). On deep palpation of this area, a firm fibrous band tissue parallel to the shaft of the femur was detected. On orthopedic examination, a continuous grade 3 (scale of 1–4) lameness on the right hind limb at walk was observed, with a lack of extension and an internal rotation of the stifle during the swing phase of the gait. The dog was unwilling to run.

Figure 1
a — Caudal view of the affected rear limb of the dog. Note the atrophy of the lateral aspect of the distal part of the caudal thigh (white arrow); b — medio-lateral radiograph of the left femur showing a band of mineralized tissue in the ...

Serum biochemical tests revealed high levels of alkaline phosphatase (ALP) (290 U/L; reference range: 25 to 110 U/L) and creatine phosphokinase (CPK) (477 U/L; reference range: 30 to 360 U/L) activity, which were consistent with a muscle lesion. Radiographs of the left pelvic limb revealed a single extended mineralized opacity with irregular margins parallel to the femoral diaphysis. Topographically, this was consistent with the cranial belly of the semimembranosus muscle (Figure 1b). Ultrasound assisted biopsy was performed and submitted for histopathological examination. Grossly, samples comprised irregular small tissue fragments with a muscular-fibrous appearance containing areas of bone-like tissue. Microscopy revealed interlacing bundles of dense, fibrous connective tissue containing dense accumulations of bone. The samples from the central zones of the lesion contained proliferating mesenchymal-like cells and fibroblasts mixed with osteoblasts depositing osteoid and immature bone. Samples from the outer areas showed a thin bone shell formed by anastomotic trabeculae of woven bone being remodelled by osteoclasts and surrounded by connective tissue that compressed the adjacent skeletal muscle, which was undergoing atrophy. Affected myofibrils presented a shrunken appearance, hypereosinophilia, and loss of normal cytoplasmic striation. Some regenerative giant muscle cells were also seen. Areas of fibrosis were intermingled between affected muscle bundles (Figure 1c). X-ray and ultrasound examination did not reveal stifle joint pathologies such as cruciate ligament or meniscus injuries.

Once the diagnosis of myositis ossificans of the left semimembranosus muscle was established, the dog was treated conservatively with rest and a non-steroidal anti-inflammatory drug for 15 d (Carprofen; Rimadyl, Pfizer, Madrid, Spain), 2.2 mg/kg, BID, PO. During a 6-month follow-up, the pathology showed no progression and clinical signs remained unchanged.

Kinematic gait analysis was performed to quantify the gait compensations that this condition induced. Pelvic limb kinematic gait analysis was also performed on 3 sound adult Doberman pinschers concurrently. Adhesive reference marks were affixed to the skin overlying the left greater trochanter of the femur, lateral collateral ligament of the stifle joint, lateral malleolus of the tibia, and over the distal point of the 5th metatarsal bone for each animal. The dogs were led by the same handler at walk from a lateral plane. Two posts, measuring 1.2 m in height and graduated every 0.1 m, were placed at 3 m intervals along the line of displacement of the animals and used as references in calibrating distances. The dogs were recorded using a 50 Hz video camera (Canon, USA) with a shutter speed of 1:250; the camera was placed 5 m perpendicular to the displacement line. The zoom was set at a position that allowed both reference posts to be seen.

From the video files, 10 samples from the frames that captured 10 complete strides were randomly selected for each dog for analysis. Linear, temporal, and angular parameters were calculated from the stifle and hock joints using a semi-automatic analysis system (SMVD; Anatomy and Comparative Pathology Department, University of Cordoba, Cordoba, Spain). These parameters included stride, stance phase, and swing phase duration, stride length, angular values as maximum (maximal extension) and minimum (maximal flexion) angles reached through the stride, angular range of motion (ARM), and Pmax and Pmin (expressed as the percentage of total stride duration at which maximum and minimum values occurred, respectively). Angular values, when the swing phase began (take off ) and when limb elevation was maximal (max elev), were also calculated. The caudal aspect of the stifle was considered to measure the angles, so smaller values meant flexion and larger values meant extension. In the hock, angles were measured from the cranial aspect, so as with the stifle, smaller values meant flexion and larger values extension.

Tables 1 and and22 show the mean values and standard deviations (s) of these variables for the sound dogs and for the lame dog. An analysis of variance (ANOVA) was carried out for each variable to compare the mean values for each dog. A Scheffé test was used to compare the mean value of the 3 sound dogs with that of the lame dog and in each case that had significance.

Table 1
Mean ± standard deviation (s) of the linear and temporal parameters of gait of the 3 sound dogs (reference) and the lame
Table 2
Mean ± standard deviation (s) of the angular parameters of stifle and hock joints of the 3 sound dogs (reference) and the lame dog during the complete stride

All but two of the parameters showed statistically significant differences, although some of them can be considered of very little importance due to their small size; thus these results could be considered as “similar.” The two variables that did not show significant differences between dogs were swing duration (P = 0.438) and maximum values in the hock joint (P = 0.987).

Mean speed (m/s) was similar in both groups of dogs (1.3 ± 0.07 versus 1.4 ± 0.07), while the stride length (cm) and stride duration (s) were shorter in the lame dog (98 ± 0.2 versus 105 ± 0.2 and 0.73 ± 0.03 versus 0.83 ± 0.03, respectively), due to its shortened stance phase duration (s) (0.39 ± 0.03 versus 0.48 ± 0.03). There were no differences in mean swing phase duration (s) between sound and lame dogs (0.35 ± 0.03 versus 0.34 ± 0.03, respectively). It should be emphasized that the minimum angle during the gait was shorter in the lame dog (115.4 ± 1.2) between the angular parameters of the stifles, which produced an increase in the value of the ARM (39.9 ± 1.1), although the maximum was greater in sound dogs (158.9 ± 1.8 versus 155.3 ± 1.1). Similar results were obtained comparing the results in the hock joint between sound and lame dogs with the exception of the maximum values, which were almost identical (155.7 ± 1.2 versus 155.6 ± 155.6 ± 1.7). Finally, the angles of both stifle and hock joints at the take-off were smaller in the lame dog (139.0 ± 1.5 and 151.9 ± 1.3, respectively). A “secondary” peak of extension was observed at 75% of the stride in the stifle of the lame dog, when the limb was within the swing phase. These results are shown in Figure 2.

Figure 2
Mean angle-time diagram of the stifle and hock joints of the 3 sound dogs (used as reference points) and the values for the lame dog. Note the secondary peak of extension of the stifle (*).


Myositis ossificans is a very rare muscular disease in dogs. Clinical examination provides useful signs for diagnosis. Biochemical tests (such as CK enzyme) allow a diagnostic suspicion of muscle injury. However imaging techniques [X-ray, ultrasonography, and magnetic resonance imaging (MRI)] and examination of pathological tissue allow a definitive diagnosis to be made.

Kinematic gait analysis has been shown to provide objective, quantifiable, and reproducible information on normal and abnormal gait in dogs (8). Studies evaluating the kinematic gait compensations afforded by specific musculoskeletal diseases, however, are few in number (1014). To the authors’ knowledge, there are currently no studies quantifying the kinematics of dogs affected by myositis ossificans.

The gait compensations observed from semimembranosus myositis ossificans in this case report are from a single dog and thus categorical conclusions or inferences from these data cannot be made. In addition, it should be noted that the kinematic profile could be different in dogs of different conformations or breeds. In this sense, the study herein represents an essential first step in defining and quantifying the kinematic alterations in dogs with myositis ossificans.

The results obtained regarding modifications in stride length, stride duration, and ARM are very similar to those reported in horses with this pathology, where a lack of extension of the stifle during stance and hyperflexion of both the stifle and hock joints have been described (1,15). Our data revealed a shortened stride length of the affected limb suggesting an inability of the fibrosed, ossified, and contracted semimembranosus muscle to reach maximal physiologic length when relaxed. In addition, a secondary peak of extension was observed during the swing phase, which may be interpreted as a conscious attempt by the dog to reach the normal angle of extension.

Variations obtained in the angular values in this case were highly demonstrative of the altered dynamics of both stifle and hock joints. The ARM was larger and the minimum angle was shorter in the lame dog than in sound dogs. Moreover, the maximum angle was shorter in the stifle of the lame dog than in sound dogs, while there was no difference in the hock of both groups. Although stance phase duration was shorter in the lame dog compared with control dogs, this is not necessarily due to a painful walk, and could be attributable to a lack of extension of the stifle of the affected limb.

Other authors have published kinematic parameters regarding pathologies such as cranial cruciate ligament rupture in dogs belonging to various breeds (11); these authors reported similar results such as the lack of extension of the femorotibial joint, but in our case, a secondary peak of extension was present during the swing phase of the stride. In addition, dogs with cranial cruciate ligament rupture show a greater angle of extension in the hock joint, contrary to what happened herein.

Variation of limb kinematics in dogs with hip dysplasia seems to be more discrete (10), and mainly affects the coxofemoral joint. Measurements from this joint were not obtained, but in future, data from the hip joint could be also relevant. We agree with the notion that body morphology is likely a major determinant of baseline kinematics in dogs (8). The most reliable data can be obtained by comparing results of normal and abnormal dogs of the same breed.

In this case report, a preliminary kinematic profile was obtained for a single dog with myositis ossificans. The findings, in combination with future cases, may facilitate formation of a gait signature to facilitate diagnosis and monitor progression of this disease. The statistical analyses should be considered cautiously, because the data are derived from a unique dog, so we can not readily extend our results to the population of affected dogs. CVJ


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1. Stashack TS. Lameness. In: Stashack TS, editor. Adam’s Lameness in Horses. 4th ed. Philadelphia: Lea & Febiger; 1987. pp. 486–779.
2. Dabareiner RM, Schmitz DG, Honnas CM, Carter GK. Gracilis muscle injury as a cause of lameness in two horses. J Am Vet Med Assoc. 2004;224:1630–1633. [PubMed]
3. Lewis DD, Shelton GD, Piras A, et al. Gracilis or semitendinosus myopathy in 18 dogs. J Am Anim Hosp Assoc. 1997;33:177–188. [PubMed]
4. Devor M, Sørby R. Fibrotic contracture of the canine infraspinatus muscle: Pathophysiology and prevention by early surgical intervention. Vet Comp Orthop Traumatol. 2006;19:117–121. [PubMed]
5. Spadari A, Spinella G, Morini M, Romagnoli N, Valentini S. Sartorius muscle contracture in a German shepherd dog. Vet Surg. 2008;37:149–152. [PubMed]
6. Turner S. Diseases of bones and related structures. In: Stashak TS, editor. Adams’ Lameness in Horses. 4th ed. Philadelphia: Lea & Febiger; 1987. pp. 293–338.
7. Dueland RT, Wagner SD, Parker RB. Von Willebrand heterotopic osteo-chondrofibrosis in Doberman pinschers: Five cases/1980–1987. J Am Vet Med Assoc. 1990;197:383–388. [PubMed]
8. DeCamp CE. Kinetic and kinematic gait analysis and the assessment of lameness in the dog. Vet Clin North Am Small Anim Pract. 1997;27:825–840. [PubMed]
9. Clements DN, Owen MR, Carmichael S, Reid SW. Kinematic analysis of the gait of 10 labrador retrievers during treadmill locomotion. Vet Rec. 2005;156:478–481. [PubMed]
10. Bennet RL, De Camp CH, Flo GL, Hauptman J, Stalich M. Kinematic gait analysis in dogs with hip dysplasia. Am J Vet Res. 1996;57:966–971. [PubMed]
11. De Camp CH, Riggs CM, Olivier B, Hauptman J, Hottinger HA, Soutas-little RW. Kinematic evaluation of gait in dogs with cranial cruciate ligament rupture. Am J Vet Res. 1996;57:120–126. [PubMed]
12. Fitch RB, Montgomery RD, Jaffe MH. Muscle injuries in dogs. Compend Contin Educ Vet. 1997;19:947–958.
13. Evans R, Horstman C, Conzemius M. Accuracy and optimization of force platform gait analysis in Labradors with cranial cruciate disease evaluated at a walking gait. Vet Surg. 2005;34:445–9. [PubMed]
14. Burton NJ, Dobney JA, Owen MR, Colborne GR. Joint angle, moment and power compensations in dogs with fragmented medial coronoid process. Vet Comp Orthop Traumatol. 2008;21:110–118. [PubMed]
15. Peloso JG. Biology and management of muscle disorders and diseases. In: Auer JA, Stick JA, editors. Equine Surgery. 3rd ed. Philadelphia: WB Saunders; 2006. pp. 1112–1120.

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