Bone and Joint Dz Flashcards
Hypothesis for the cause of OSA
Circumstantial evidence only but may be to do with microtrauma in larger breed dogs
Or the effects of GH and IGGF-1 which are required for normal bone growth and homeostasis.
Risk factors for appendicular OSA
Large breeds: Rotti, Great Dane, Greyhound, Saint Bernard, Irish Wolfhound
Polygenetic germline risk factors in these breeds
Neutered dogs reported to have 2x higher risk
Key diagnostic features of appendicular OSA
Rads - cortical lysis, periosteal bone proliferation, loss of trabecular bone, pathological fractures, periosteal lifting, sunburst periosteal new bone.
Expansile, permeative or moth eaten bone loss
Distal femur or radius, proximal humerus or tibia
DDx: fibrosarcoma, osteomyelitis (fungal and bacterial), chondrosarcoma
Possibly elevated ALP
Sensitivity of different staging for Appendicular OSA
CT > thoracic radiographs for mets
Published Tx and patient outcomes are based on studies using radiographs –> so bare that in mind when reporting outcomes for metastatic disease (probably more advanced than what would be detected on CT in some cases)
Bone survey radiographs to look for distant mets - particularly if planning amputation.
Comparison of whole body CT to nuclear scintigraphy with bone tracer –> scintigraphy was most useful for occult metastasis (though false positives were reported and final diagnosis was not based on histo)
PET scans were also reported recently to have prognostic value with higher uptake of tracer associated with poorer prognosis.
Limitations of bone biopsy for dx oof OSA - Vet Path bone tumour review
Can be difficult/impossible to differentiate if there is a large amount of tumour matrix present as it could be from chondrosarcoma or fibrosarcoma.
Best are core tumour biopsies with Jamshidi which has accuracy rate of 92% for OSA
Preoperative bx can be challenging to get a diagnosis and typically cytology has been reported to be ineffective, though may be improved with ALP staining.
Histological grade was not associated with tumour behaviour in one study
Biological behaviour of OSA and prognostic factors
Highly aggressive
60% die from metastatic disease and 90% die within 1 y (if not mets then pain related)
Metastasis to lungs, LNs, skin)
MST 100-200d with amputation alone
–> not impacted by presence of metastasis on rads
One study reported a longer survival time in dogs with bone mets than those with lung mets.
Elevated ALP has been associated with poorer prognosis - especially if not normalising within 40 days of surgery
Appendicular OSA Tx options and prognosis
Amputation alone 100-200d
–> contraindicated if other limb have lameness
Limb sparing surgery can be considered for distal radius tumours and can be combined with intraoperative RT for unknown benefit
Post-op infections associated with improved prognosis though to be due to immune stimulation (anti-OSA macrophage response)
Chemotherapy adjunctive Tx is beneficial to survival when combined with Sx but not as a sole therapy. Comparative studies are largely lacking
MST 300- 400 d
Carboplatin was not superior but reported to have less adverse effects than other treatment protocols
Longer survival with ongoing metronomic chemotherapy after initial treatments may improve survival time
Palliative radiation also reported but associated with high risk of complications (post-irradiation fracture). USed as analgesia
Bisphosphonates (alendronate) - may improve pain relief through promoting apoptosis and inhibiting osteoclastogenesis and angiogenesis.
Other appendicular bone tumours
Chondrosarcoma-
can be manged with amputation as well but chemotherapy not reported to provide improved prognosis. Low metastatic potential even with prolonged follow up
Nasal chondrosarcoma have a poorer prognosis
Fibrosarcoma - amputation and adjunctive chemotherapy recommended
Haemangiosarcoma - may be primary or metastatic. Often a polyostotic disease making amputation contraindicated unless thorough staging excludes this.
Overall guarded prognosis
Axial sites of OSA and their prognosis
Mandible, maxilla, skull, vertebrae, ribs, nose and pelvis
(also rare soft tissue form)
May have less aggressive behaviour than appendicular but prognosis is dependent on ability to resect
Local recurrence is the most common cause of death
Survival was better for dogs with mandibular tumours treated with mandibulectomy (71% alive at 1 y) cf with other types of axial OSA 240d. though the majority still go on to develop metastatic disease
If resectable rib and pelvic tumours should also receive post-op chemo
Multilobular osteochondrosarcoma - behaviour and Tx
Arises from bone periosteum most often on the skull
Mineral density throughout tumour - multiple lobules each centred on a core of cartilagenous or bony matrix
Tx surgical resection and RT
–> local recurrence in up to 47% after >2y
Metastatic disease reported in 56% of dogs but with prolonged time.
Cause and Tx of bacterial osteomyelitis
Most often direct inoculation or implant infection
–> needs to be compromised bone for infection to occur. Haematogenous spread unlikely.
G+ surgical site infections are most common
G- and anaerobes after trauma/bites
Immune response to infection results in additional bone necrosis through inflammatory cytokines
Tx - ABx alone are rarely sufficient require debridement and removal of implants if present. Due to sequestra and biofilm formation being common
Clindamycin -good G+ and anaerobe coverage with good penetration of tissue but resistance is common in Staphs that are MRSP
Recommended duration of Tx is 4-6 weeks, though this is not based on prospective studies
Also consider antimicrobial impregnated materials as implants for deep infections - allow greater concentration of ABx where needed at site of infection
Benign lesions of bone
Osteomas - dense bony projections, well circumscribed and not painful
Multiple cartilaginous exostosis - developmental condition with possible heritable component
Find lesions on bones that form from endochondral ossification and stop growing at maturity when endplates close.
Can remove surgically if not resolved after skeletal maturity. Rare reports of malignant transformation
Bone cysts may be result of growth plate trauma interfering with endochondral ossification
–> often found near metaphysis of young dogs
DDx for periarticular tumours in canine
histiocytic sarcoma (can be localised); synovial myxoma
Malignant fibrous histiocytoma
synovial cell sarcoma
will need IHC to differentiate
Amputation usually recommended Tx
Staging including LN biopsy is recommended (as 33% met to LN and 91% for histiocytic sarcoma)
Reported feline bone tumours
70-80% are OSA
similar findings as dogs overall. More often occurring in appendicular skeleton. Rare extra-skeletal primary tumours are also reported.
–> less often metastasise though are locally aggressive.
Tx is limb amputation but no proven benefit of adjunctive chemo.
Ddx multiple cartilaginous exostosis; chondrosarcoma
–> MCE may have viral origin and tends to affect affect axial skeleton (scapula, vertebrae, mandible). Can be rapidly progressive and cause hard swellings
–> carries a guarded prognosis due to rapid progression of lesions
What causes nutritional secondary hyerPTH and what are the symptoms and Tx
Chronic insufficient Ca intake (or high PO4 intake)
–> increased PTH production
–> increased bone resorption to maintain serum Ca
–> excessive osteoclast activity and pathological fracture of young bones
Does not effect growth plates or mineralisation of osteoid
High PTH, normal iCa and high Vit D
(Can see concurrent Vit D deficiency if all meat diet)
Aim for Ca:PO4 of 1.2:1 andensure absolute amount of Ca in food is adeuqate.
Improved mineralisation of the skeleton should be evident at 3-4 weeks, as almost 100% of the Ca will be reabsorbed due to high hormone levels
Causes of Rickets and clinical signs/Tx
Hypovitaminosis D - can be poor intake due to deficient diet (ie all meat)
Congenital:
Type 1 defect in renal conversion enzyme CY27B1 or the liver conversion enzyme CYP2R1resulting in reduced calcitriol production\
Type 2 - defect in Vitamin D receptor resulting in resistance to Vit D effects
All result in defective mineralisation of new bone and cartilage –> METAPHYSEAL THICKENING (differentiates from Ca deficiency or P excess where growth plates are not affected)
Type 1 Rickets and low intake can be corrected by supplementation of calcitriol/Balancing Ca intake and PO4 in diet.
Type 2 Rickets is not responsive to Ca supplementation so requires high dose Ca supplementation
What is panosteitis and what causes it
Painful condition of the long bones in large breed growing dogs.
Usually resolves with cessation of growth (may be up to 2y in age)
Increased occurrence in male dogs compared to females. Typically larger breeds but not always
Can cause a shifting lameness +/- fever. Pain lasts 2-5 weeks, but is recurrent and often changes legs
Rads - characteristic bone marrow cloudiness. Scintigraphy is required for definitive Dx
Caused by replacement of fatty marrow with fibrous tissue which is then replaced by woven bone
–> eventually normal bone remodelling takes over and dissolves this bone.
The inciting cause for this process is not known - currently thought that high protein diet may contribute.
Possibly a genetic basis due to breed predilections (GSD, Golden Ret, BAsset Hounds, Doberman, Labradors)
DDx hypertrophic osteopathy, osteomyelitis, IMPA
Hypertrophic osteodystrophy - JSAP 2022 review, typical presentation and diagnosis
Same as metaphyseal osteopathy
Autoinflammatory disorder of unknown aetiology - may be associated with vaccination, CDV, hereditary or autoimmune.
–> blood flow to part of bone is reduced and interrupts normal bone formation
At risk breeds: Kelpie, Boxer, Doberman, GSD, Great Dane, Iris Setter, Irish Wolfhound, Labrador, Rotti, Weimaraner
Similar demographic to panosteitis but HOD typically affects >1 limb at a time unlike panosteitis. HOD is often more painful and can result in permanent growth plate damage.
Present with pain and swelling often distal radius/ulna, loss of appetite, fever
–> symmetrical metaphyseal swelling
Also reportd to have diarrhoea, pyoderma, oculo-nasal discharge, increased bronchovesicular sounds, haematochezia, valvuvaginitis
And in severe cases SIRS symptoms due to inflammatory cytokine cascade
Diagnosis of HOD
Patient <15 months
Swollen metaphysis of long bones or mandible
Systemically unwell, febrile +/- nasal discharge or tachypnoea or increased bv sounds
Radiograph double physeal sign (radiolucent line parallel to the physis (most evident in distal radius/ulna)
Screening for infectious disease is advised especially if concurrent respiratory signs or
DDx infectious disease CDV, pneumonia, parvovirus, tick-borne infections, IMPA, septic arthritis (single limb); nutritional hyperPTH
Recommendations for Tx of HOD and evidence
Limited evidence for any particular Tx
Mild cases often do well with just NSAIDs and activity restriction
Moderate or severe cases may need hospitalisation for management of nutrition and analgesia while awaiting response to steroids/NSAIDs
A comparative study reported that HOD treated with steroids resulted in faster recovery of symptoms compared to NSAIDs, and also that those not responding to NSAIDs would then respond to steroids.
–> risky due to possibility of infectious cause in such a young dog and also impact that steroid administration may have on growth overall
Prophylactic coverage with ABx may be considered if there is concern for infectious aetiology and awaiting cultures
JSAP 2023 39 case series - median hosp duration was 5 days
Half treated with steroids, the others NSAIds, some failed NSAID and changed
8/25 with long term follow up relapsed before skeletal maturity was reached.
4/25 with follow up developed immune mediated coditions
Effects of hypervitaminosis A
Seen more in cats due to inability to excrete large amounts of retinol in urine
–> diets high in offal such as liver predispose to excess
Vit A promotes new bone formation without osteolysis
particularly at ligament insertion points.
In excess it also inhibits collagen synthesis and provokes breakdown of musculotendinous insertions in the periosteum during normal muscle activity
(though in cats to be cervicothoracic spine due to grooming movements)
–> in severe cases results in cervical immobilisation and scoliosis of cervical spine. Inability to turn head/neck and is painful on manipulation.
–> may see lameness due to compression of intervertebral foramen where nerves exit spine
In kittens may also see loosening of teeth, damage to epiphyseal long bone plates, oedema or inflammation of gingiva
Changes are irreversible but modification of diet prevents progression
–> neuropraxia that develops may improve with diet change but skeletal changes are irreversible.
Poor prognosis for functional recovery.
