Panosteitis

Panosteitis is one of the most common causes of lameness in young, large breed dogs, and is common worldwide [1-20]. Panosteitis is a self-limiting disease of the bone marrow of long bones in which the adipose and hematopoietic tissue is temporarily replaced by fibrous tissue [1-20]. Osseous changes also occur affecting the trabeculae, endosteum, and in more severe cases, the cortex and periosteum [4,15]. Pain and lameness of the affected limb(s) are the consistent clinical signs that last 2 weeks or less [4,15]. Panosteitis typically recurs episodically, and is the classic cause of "shifting leg lameness" [4,15]. It is unusual for panosteitis to affect the same bone twice (1%), but it can affect the same leg multiple times [4]. Clinical signs of panosteitis are uncommon after 18 months of age, although in one study 18% of the patients were older than 18 months [4]. Panosteitis spontaneously regresses, so treatment is usually limited to short-term administration of NSAIDs or corticosteroids as needed for adequate pain control.

Synonyms for panosteitis include: enostosis, eosinophilic panosteitis, juvenile osteomyelitis, and canine panosteitis [9,15]. Enostosis is defined as "morbid bony growth of endosteum or within the medullary cavity" [14]. This, along with fibrosis and destruction of normal medullary cellularity, describes the most common pathologic features of panosteitis [4,15]. Early reports of panosteitis were associated with eosinophilia, but subsequent reports indicate only 1% to 5% have eosinophilia [4,9,15]. Juvenile osteomyelitis is a misleading nomen (see Etiology). Canine panosteitis is redundant because, to the authors' knowledge, it has only been reported in dogs [15]. Panosteitis is the commonly used name. One sage author has proposed that any name change should await definitive identification of the etiology [4].

Panosteitis was first described in 1951 in young German shepherd dogs in Europe [15]. Panosteitis was reported in the United States in 1960, and was reported to spread rapidly [15]. However, the "spread" of panosteitis is thought to be a more the result of increased awareness than epidemiologic spread [15].

Etiology

The etiology of panosteitis is unknown [2,15]. Along with HOD and cranial mandibular osteopathy, panosteitis is a disease of unknown etiology in juvenile dogs that is characterized by osseous proliferation and excessive bone remodeling [9]. However, panosteitis is a unique disease with characteristics unlike any other known disease [4].

Proposed etiologies for panosteitis include bacterial infection, viral infection (e.g., distemper), genetics, stress, metabolic disease, vascular anomalies, allergy, hyperestrinism, parasite migration, autoimmune reaction after viral infection, and hemophilia [3,13,15]. Some reports of potential etiologies had convincing circumstantial evidence, but subsequent cases did not support the connection. Medical advances (e.g., improved microbiology diagnostics, parasite control, vaccines, etc.) have made several proposed etiologies unlikely. Other proposed etiologies remain possible, but proof is lacking. Attempts to isolate causative infectious agents from dogs with panosteitis have been unsuccessful [20].

Bacterial infection was the originally proposed etiology [15]. Panosteitis was thought to be a result of purulent hematogenous osteomyelitis caused by streptococcus [15]. However, necropsy of 18 dogs failed to identify any bacteria at the lesions [9,18]. Other studies also reported negative cultures associated with panosteitis lesions [4]. The few blood and bone marrow cultures have been negative for aerobic and anaerobic bacteria [15]. Histopathology consistently fails to implicate a bacterial etiology, and WBC counts are typically normal [4,15]. Antibiotic therapy is ineffective [15]. Furthermore, the long clinical history with panosteitis does not support a readily contagious agent as the sole cause [1-20].

Viral etiology has been strongly supported by some authors [9], and it remains a potential cause. Initial reports of panosteitis in 1951 roughly corresponded to the common use of live distemper vaccination, and a connection was suspected [9]. Most dogs are vaccinated against canine distemper and never develop panosteitis. Nevertheless, some authors recommend vaccination with killed distemper or adenovirus vaccine rather than modified live which may still "allow transcription into messenger RNA" [9,19]. Viral etiology of panosteitis was suggested by a report of successfully inducing panosteitis via medullary aspirates (filtered or unfiltered to remove bacteria) from dogs with panosteitis and injected intramedullary into unaffected dogs [18]. Panosteitis-like lesions were reported in the inoculated bones 2 to 3 weeks later and also developed in one bone of a marrow recipient that was not inoculated [18]. Transmission was reported to be more readily accomplished in male dogs [18]; however, the validity of this report has been questioned [15]. Host response to inoculated foreign material likely caused the observed lesions. In addition, bone marrow and buffy coat samples from dogs with panosteitis were placed in kidney cell lines without cytotoxic effects, which would refute a viral etiology [15,20]. Reports of panosteitis with concurrent clinical findings of pyrexia, tonsillitis and leukocytosis also suggest viral infection [9], however, the numerous cases of panosteitis without pyrexia, tonsillitis, and/or leukocytosis makes it likely that these signs were coincidental.

Genetic influence or cause of panosteitis is a consideration because of predilection for certain breeds (Table 95-1). Panosteitis is most common in German shepherd dogs, but can occur in almost any large breed [11]. A purely genetic cause is doubtful because so many breeds are affected (n=59 in our VMDB [1] survey. The VMDB does not give number of cases at every month, or year, of age. Cases within an age range are reported as "0-2 wks; 2 wks-; 2 mn; 2-6 mn; 6-12 mn; 1-2 yr; 2-4 yr; 4-7 yr; 7-10 yr; 10-; 15 yr; and 15 yr+". The number of cases for VMDB data in Fig. 95-1 was placed at the center of the age ranges, with cases >4 years old placed at 60 months on the chart) [9]. One report stated that English pointer pups and German shepherd pups were raised in the same pen, yet only German shepherds routinely developed panosteitis [15]. This limited report supports lack of an infectious agent even more than it suggests genetic influence.

Figure 95-1. Age distribution of dogs with panosteitis from VMDB (662 dogs) and Bohning et al. report (100 dogs) indicates panosteitis is predominantly a juvenile disease.  

Hemophilia A was reported in three male German shepherd dogs with panosteitis. Histopathologic and gross pathologic studies showed typical panosteitis plus hematomas. The signalment is the same for both diseases. However, the author stated it was "unwarranted to conclude that all dogs suffering from enostosis have bleeding disorders", but suggested that "bleeding disorders should be considered when discussing the etiology of enostosis" [13].

A frequent correlation exists between the first estrus and the first episode of panosteitis, which has led to speculation of hyperestrinism as a cause of panosteitis. Stress is thought to often precipitate panosteitis episodes [15]. Stress is a common factor in estrus, metabolic disease, allergy, parasite migration, and autoimmune reaction after viral infection, all of which have been speculated as causes of panosteitis. The inability to identify a single cause of panosteitis over 5 decades suggests that panosteitis may be caused by the confluence of multiple factors.

Pathology

Panosteitis is a self-limiting disease of the metaphysis and diaphysis of long bones of juvenile dogs, predominantly large breeds [4,15]. Panosteitis has never been reported to affect the epiphysis [15]. Panosteitis begins with loss of medullary adipose tissue, followed by fibrous proliferation, intramembranous ossification, osteoclastic removal of trabeculae, and in more severe cases, periosteal proliferation and cortical changes [9,11,15]. The process then regresses to normal or near normal architecture in the vast majority of cases [15]. This cycle is typically 60 to 90 days, but may be up to 190 days [3,15,16].

Panosteitis has been characterized as a disease of adipose bone marrow with secondary osseous effects [15]. As supportive evidence, the reaction to fractures and to irradiation to remove bone marrow are examples given of adipose bone marrow damage, with histologic and radiographic responses similar to panosteitis [15]. In addition, these events also follow a 90-day pattern [15]. Pathology begins with vascular leakage of protein-rich edema from congested medullary blood vessels and degeneration of adipose tissue [3,9,11,15,16]. Increased leucocytes and plasma cells are typically not observed [2,4,9,17].

As the edema quickly organizes, fibroblastic reticular cells of bone marrow stroma produce a marked and highly cellular fibrosis in the medullary canal [2,4]. Hematopoietic tissue is replaced by massive amounts of fibrous tissue, which is rich in fibroblast, osteocytes, osteoblast, and osteoclast, but which is usually not inflammatory [4,9]. Osteoclasts remove much of the preexisting trabeculae, which are replaced by formation of a haphazard trabecular system of woven bone [4,9,15]. These new trabeculae tend to be short and thick, and may obliterate the medullary canal [9]. In addition, areas of acellular calcified material and intramembranous woven bone are scattered throughout the medullary cavity [2,4,15]. High osteoblast and fibroblast activity also occurs along the endosteum, and in some cases, the cortex and periosteum [3,4,16]. Cortical bone may be replaced with woven bone, especially around the nutrient foramen, and appear as a zone of decreased density [9]. Hyperemia of periosteum and adjacent soft tissues commonly provokes a mild periosteal reaction that may not be detected in most dogs, but can result in periosteal new bone a few millimeters thick [2].

During late stages, woven bone trabeculae are replaced by fewer lamellar bone trabeculae, which tend to be fewer and thicker than normal [15]. Remnants of the pathologic changes may persist for months [2,4]. Components of the histologic appearance of panosteitis are not unique or pathognomonic (e.g., also seen at borders of bone tumors and focal bone infections) [2]; however, no evidence of inflammatory cell exudate, necrosis, or neoplasia exists [2,17]. The amount of remodeling varies between dogs and even between episodes [9]. Repeated attacks make marrow aplastic, with little to no hematopoietic bone marrow [15].

Clinical Diagnosis

Signalment

The quintessential case of panosteitis is a 10-month-old male German shepherd dog. Although the signalment has strong predispositions, the range of breeds and ages represented is broad. Ranges of and predispositions for age, breed, and gender were determined for this chapter by literature review and a retrieval from the Veterinary Medical DataBase, including all participating institutions, and from 1994-2004 inclusively. Cases per 100,000 were calculated for breeds with more than 1000 in the total population.

Age

The majority of panosteitis patients are 5 months to 12 months old; however, the age range is 2 months to 5 years old and older. The VMDB survey for this chapter had 662 cases of panosteitis, of which 380 dogs (57%) were 6 to 12 months old.* This VMDB survey further indicated that 64% were ≤12 months old, and 89% were ≤2 years old (n=590). The VMDB survey had a case at 2 months old, but also reported 14 cases between 7 years old to more than 15 years old (2%) (Fig. 95-1).

The literature cites age ranges typical for panosteitis from 5 months to 12, 18, 20, or 24 months old [3,4,11,15]. An excellent 1970 study of 100 consecutive cases of panosteitis reported the peak occurrence was at 9 months and 10 months (n=14 each month) (Fig. 95-1). This study also reported that 71% were 5 to 12 months old, 82% were ≤18 months old, and 95% were ≤2 years [4]. The reported mean age at initial diagnosis was 12 months 2 weeks old, but the mean calculated from their data by this author was 10 months old [4]. Female German shepherds accounted for the single cases at 2 months and 5 years old [4]. The second youngest was 5 months old (n=7), and the second oldest was 30 months old (n=2) [4]. Hence, the age range or mean that constitutes "typical" depends on what percentage of cases is included. Results of the VMDB survey for this chapter and the 1970 study of 100 dogs with panosteitis are comparable (Fig. 95-1).

Breed

German shepherds are most commonly afflicted with panosteitis, whether based on the number of cases, % of all cases, or cases per 100,000 of the breed (Table 95-1). Our VMDB survey indicated German shepherds had the most cases (n=259), the highest percentage of cases (39%), and the highest risk (2053 cases of panosteitis/100,000 German shepherds). A 1970 study of 100 consecutive cases of panosteitis had 79% German shepherds [4]. An earlier VMDB survey is the only report with German shepherds having the second highest number of cases (n=648); mixed breed dogs had the most cases (n=945) [1].

Basset hounds had the second highest risk (1999 cases/100,000 bassets), were tied for 3rd most cases with 53 (Table 95-1), and accounted for 8% of all cases in our VMDB survey. Labrador retrievers had the second highest number of cases with 72 and accounted for 11% of all cases, but had lower risk with 238 cases / 100,000 Labrador retrievers (Table 95-1).

Eight breeds (Table 95-1) account for 81% of all cases of panosteitis in our VMDB survey. These or similar lists of prevalent breeds being previously reported [1-4,8,9,15]. Panosteitis occurred in 59 breeds in our VMDB survey, but 25 breeds had only 1 case. Twelve breeds, including mixed breeds, had fewer than 100 cases/100,000 of the breed, indicating low risk.

Small breeds with panosteitis had a total of 12 cases, or 1.8% of all dogs with panosteitis, in our VMDB survey. Cardigan Welsh corgis had the most cases with 3, blue heelers accounted for 2 cases, whereas the American cocker spaniel, Maltese, Norwich terrier, miniature schnauzer, Shetland sheepdog, Pembroke Welsh corgi, and wirehaired pointing griffon had 1 case of panosteitis each. A previous study likewise reported 99% of dogs with panosteitis were large breed (Miniature Schnauzer was the exception) [4].

Gender

The predilection for males to have panosteitis is consistent and noteworthy. Our VMDB study showed males accounted for 70% of all cases of panosteitis, yet the overall population was only 48% males. Males account for 67% to 84% of all cases of panosteitis based on the literature [3,4,6,11,12,15]. One study of 100 dogs with panosteitis had 79% males, with German shepherds and 1 Saint Bernard accounting for all the females [4]. Panosteitis recurrences have been reported to be more predictable in males [15]. Females usually have the first episode of panosteitis associated with the first estrus [15].

Patient History

An acute onset of mild to moderate lameness is the typical history, although severe lameness is also commonly reported [4,9,11,15]. Duration of lameness is up to 14 days (rarely, 3 weeks in severe cases), although lameness from panosteitis is often as short as 2 days [2,4,9,15]. Decreased appetite and activity may be reported coinciding with the lameness [2-4,11,12]. Lameness is not affected by rest or exercise, but lameness usually increases during the first few days of an episode [15]. Pain is most likely from stimulation of pain receptors in the periosteum and/or owing to medullary hyperemia and congestion [2]. The initial episode of panosteitis most often affects a front leg, followed by rear leg, then returns to a front leg [15]. "Shifting leg lameness" is a classic historical description for panosteitis (see Prognosis for more detail) [2,3,9,11,12]. Lameness can also affect one or more legs simultaneously or sequentially (Fig. 95-2) [2,4,15]. The initial onset of lameness owing to panosteitis is uncommon (~10%) over 2 years of age (see Signalment for more detail) [4,15].

Figure 95-2. Radiographic signs of panosteitis evident in the humerus, radius and ulna of the same leg (arrows). The ulna has the earliest radiographic signs (see insert) of radiolucency at the endosteal surface. The later radiographic sign, which is most often the first appreciated, is radiodensity of the medullary canal which is patchy (humerus) or generalized (radius).

Examination Findings

Lameness ranges from mild to non-weight bearing [15]. Diagnosis is primarily via palpation [15]. Pain of affected bone is exacerbated and localized by deep palpation of the bone, with painful responses ranging from mild to severe [2-4,9,11,12,15]. Panosteitis tends to start at the nutrient foramen (approximately at the junction of the proximal third with the distal two thirds of long bones), but panosteitis can also occur elsewhere in the diaphysis or metaphysis [4,9,12,15]. Care should be taken not to compress soft tissues, other than skin, to avoid a false positive response. Panosteitis is easily overlooked, and probably often, unless direct palpation of long bones is a routine part of the orthopedic examination for dogs at risk [4]. Muscle atrophy is rarely present owing to panosteitis because of its acute onset and short duration of clinical signs [4]. Confirmation via radiographs is recommended, although initial radiographs may only rule out other etiologies [3,4]. One report indicated minimal radiographic signs in 5 of 100 dogs with panosteitis [4]. In addition, radiographic signs of panosteitis may not be observed for 10 to 14 days after onset of clinical signs, yet there may be more sensitivity during the first few days (i.e., the patient may be more likely to be presented for examination) [2,12,15]. A poor correlation exists between severity of clinical signs and radiographic changes with panosteitis [2,4,9,11,15].

The most commonly affected bone differs among reports. One report lists in descending order the ulna (42%), radius (25%), humerus (14%), femur (11%), and tibia (8%) [15]. A different report lists the most commonly affected bones as the humerus (68%), femur (68%), ulna (54%), radius (27%), and tibia (24%) [4]. The latter reported panosteitis of the contralateral bone in 31% (humerus) to 60% (tibia) of the cases, with only 1 of 100 dogs having panosteitis in the same bone more than once [4]. Different phases of the disease may be occurring concurrently in the same dog at the same time (Fig. 95-2) [15].

Concurrent orthopedic diseases are common (26% in one report) [4] in dogs with panosteitis [2-4,9,11,15]. Hence, a complete orthopedic examination, and radiography as indicated, should always be performed. Other findings are rare, but may include pyrexia, anorexia, tonsillitis, eosinophilia, muscle atrophy, and elevated white blood cell counts, none of which are unique to panosteitis [3,4,9,15]. Fever, anorexia, tonsillitis, and eosinophilia have each been reported to occur in only about 1% of panosteitis cases [4,9]. Most cases of panosteitis are in otherwise healthy dogs [3].

Radiographic Findings

Four radiographic stages are associated with panosteitis, three of which are commonly observed. These stages are in reality a continuum of pathology, and various authors differ on the arbitrary points of delineating stages. The radiographic stages of panosteitis are 1) radiolucency of the medullary canal, 2) radiopacity of the medullary canal, 3) endosteal, cortical, and periosteal reaction, and 4) recovery.

The earliest radiographic sign of panosteitis is increased radiolucency of the medullary canal (Fig. 95-2) [4,8,12,15]. The radiolucency corresponds to the early pathologic changes to medullary adipose tissue, occurs early, and is rarely observed [2,12,15]. Radiolucency can be recognized 10 to 14 days after onset of clinical signs [12]. High quality radiographs are necessary to see changes that are present when clinical lameness begins [9]. If uncertain, additional radiographs should be taken 2 to 3 weeks later to show more obvious changes [9].

The second stage of radiographic change, and typically the first observed, is increased density of the medullary canal in a patchy or mottled pattern, most frequently starting near the nutrient foramen (Fig. 95-3) [4,11,12,15]. The radiopacity corresponds to the pathologic changes of proliferating stromal and adventitial cells in the medullary canal, and their subsequent calcification and intramembranous bone formation [2,9,12,15]. This radiographic stage typically begins 10 to 14 days after initial clinical signs [15]. Initially, these changes can be subtle (Fig. 95-2) [9]. Radiographic changes of this stage usually last 4 to 6 weeks [4]. Consistent early changes in this stage are loss of normal trabecular pattern, loss of medullary-cortical contrast (owing to increased medullary radiodensity), plus a variable number of intramedullary granular densities [3,4,9]. Early changes that may also be observed are accentuation of the trabecular pattern prior to or adjacent to increased medullary radiodensity, and the cortical changes around the nutrient foramen which accentuates the foramen (Fig. 95-2 and Fig. 95-3) [4,9]. Midway in this radiographic stage the appearance is patchy or mottled, with sclerotic densities of various size and extent [3]. Granular density can be seen in the medullary canal early to late in this stage [4]. Homogenous radiodensity fills the medullary canal in some cases [4]. As this stage progresses toward the next, the endosteal surface becomes roughened, with coarse trabeculae extending into the medullary canal [4]. In about a third of cases, usually those with extensive medullary involvement, periosteal roughening is followed by periosteal new bone (Fig. 95-4) [4].

Figure 95-3. A. Discrete patchy area of medullary radiodensity characteristic of panosteitis which is later than seen in the ulna of Figure 95-2. B. Radiodensity of the medullary canal of the radius is patchy and limited in area, compared to the more advanced humerus which is patchy but nearing generalized radiodensity of the entire diameter and over a larger area.  

Figure 95-4. A. Radiodensity of the medullary canal typical of panosteitis has progressed from patchy and limited areas, as seen in Fig. 95-3, to involve almost the entire length of this tibia. B. This tibia has medullary radiodensity plus the periosteal proliferation, indicating even further progression compared to Fig. 92-94A. Not all dogs with panosteitis progress to this severity of radiographic changes.

The third radiographic stage, typically the second observed, includes endosteal, cortical and periosteal reaction (Fig. 95-2 and Fig. 95-4). The radiographic signs of endosteal, cortical, and periosteal bone changes correspond to the pathologic changes described for the previous stage and formation of woven bone that progress to affecting cortical bone [9]. There is continuation of the obvious patchy or mottled radiodensity, and often an increased radiodensity approaching that of the cortex [4,9]. Endosteal roughening and then periosteal roughening may precede new bone formation, and a coarse trabecular pattern may be present [9,15]. Periosteal new bone is seen in 15 to 25% of affected cases, ostensibly the more severe cases [2]. Periosteal and endosteal new bone yields the appearance that the cortex is thicker in that region and margins are indistinct [9]. Cortical bone may be replaced with woven bone in some areas [9]. Cortical osteoporosis, if seen, is due to enlargement of the osteonal canals [15]. Thickening of areas of the cortex occurs in about a third of cases [4]. Radiographic diagnosis of panosteitis is easiest in this stage [4].

The fourth radiographic stage, typically the third observed, is recovery. The radiographic signs correspond to the reversal of the pathologic changes, plus evidence of residual changes. These changes include a decreased number of granular densities, return to normal medullary appearance, and cortical and trabecular remodeling, with regression toward the nutrient foramen (reverse order of formation) [2,3]. The medullary canal progresses to a more normal appearance over a 2- to 3-month period [9]. Regression of bony changes is via osteoclastic removal of trabeculae that do not serve a biomechanical function, and requires months [2]. Persistent changes can include slightly increased density of the medullary canal, granular densities, fewer and coarser trabecular bone, roughened endosteum, and increased cortical thickness (Fig. 95-5) [2,4].

Figure 95-5. Fewer and courser trabeculae are long term radiographic indicators of prior panosteitis in this humerus. NOT all episodes of panosteitis have as severe, or any, chronic radiographic changes. These changes are seen after the clinical signs of panosteitis.

The severity and extent of radiographic changes with panosteitis varies greatly [2,4,15]. The overall cycle of radiographic changes for a given bone with panosteitis is typically 60 to 90 days, but may last up to 190 days [3,15,16]. Different stages of panosteitis often occur concurrently in the same dog at the same time (Fig. 95-2) [2,4,15]. One study reported radiographic changes consistent with panosteitis in 2 or more bones at the same time in 24 of 25 dogs that had radiographs of all limbs [4]. As many as 7 bones have been affected at one time by panosteitis [15]. Radiographic changes owing to panosteitis often center around the nutrient foramen [4,9,12,15]. One report stated that changes affect the diaphysis only in 75% of dogs, with extension to include the metaphysis in 25% of dogs [4]. There has not been a report of panosteitis affecting the epiphysis [15]. Panosteitis affecting the same bone twice is rare (1%) [4]. Repeat episodes of panosteitis can result in bones becoming cuboidal and "lose their graceful appearance" owing to repeated remodeling [15]. Although panosteitis almost always affects the long tubular bones, 1 dog was reported to have radiographic lesions typical of panosteitis in the ilium [4].

Treatment

Because panosteitis is self-limiting, with clinical signs limited to lameness because of pain, appropriate therapy is typically limited to NSAIDs. Treatment can be on an as-needed basis for the duration of clinical signs, which may be as short as 2 days to as long as 3 weeks [2,4,9,15]. Aspirin has been frequently recommended, but other NSAIDs would also be appropriate [4,9,15]. Corticosteroids may be used in refractory or severe cases [2,15]. Other analgesics may be used but are rarely necessary [15]. Exercise or rest does not affect the severity of lameness [15], although two reports suggest restricted activity as part of the treatment [2,9]. Concurrent orthopedic problems or other signs (e.g., anorexia) are treated separately [2,3].

Other treatments that have been tried with minimal success include antibiotics, vitamin and mineral supplements, dietary changes, and irradiation of diseased bone and adrenal glands [15].

Prognosis

The prognosis for a given episode of panosteitis is excellent. Lameness and pain last from 2 days up to 3 weeks, with or without treatment [2,4,9,11,15]. However, pain may be severe, and even less than severe cases warrant pain relief. Medications such as NSAIDs or corticosteroids almost always provide excellent relief from clinical signs. The severity of attacks tends to decrease as age increases [15].

The long-term prognosis for panosteitis is also excellent [2,4,9,11]. However, recurrences are common in dogs up to about 18 months old [2-4,15]. Approximately 5 to 11% of panosteitis cases occur in dogs over 2 years old (Fig. 95-1) [4]. Although it is rare for panosteitis to afflict the same bone a second time (1%), panosteitis will often afflict one or more other long bones in the same or different legs [4].

The initial episode of panosteitis most often affects a front leg, followed by rear leg, then returns to a front leg [15]. "Shifting leg lameness" is a classic historical description for panosteitis [2,3,9,11,12]. In many cases lameness shifts every 2 to 4 weeks, with lapses of up to 1 month or more [4,9,15]. The frequency of recurrence has been reported to be more predictable in males [15]. It is not uncommon for a dog to have 1 or just a few episodes, rather than repeated and frequent episodes up to age 18 to 24 months; at least not enough episodes affecting the dog for veterinary attention to be sought. In a report of 100 consecutive dogs with panosteitis, multiple leg involvement occurred in 49%, and multiple bone involvement in 53% [4]. Multiple leg involvement was equally distributed between front and rear legs [4]. Lameness can also affect one or more legs simultaneously [4]. The frequency and severity of clinical lameness tend to decrease with age [15].