The spontaneous rupture of the cranial cruciate ligament in dogs remains a pathoetiologic puzzle. Despite much progress in research over the past years, the systemic and local mechanisms leading to ligament degeneration and structural failure remain largely obscure. This scoping review focuses on pathogenesis and aims at summarizing and interpreting today’s knowledge on causes of canine cruciate ligament rupture, i.e., the multifactorial mechanisms leading to degenerative stifle joint disease with collagen matrix degeneration and structural failures. Thus, the initial view of traumatic ligament rupture, fostered by “wear and tear”, has clearly been replaced by a new concept of systemic processes linked to progressive degenerative joint disease and ligament failure; thus, the term “cranial cruciate ligament disease” has been coined and is generally accepted. In addition, cruciate ligament rupture in people shares some similarities with the lesion in dogs; therefore, the review also includes comparative studies. The methods used were based on the PRISMA-ScR model (Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews).

The etiology of spontaneous cranial cruciate ligament rupture in dogs is unknown despite being one of the most impacting orthopedic diseases in dogs. Numerous studies have contributed to the understanding of a multifactorial pathogenesis, this, however, without identifying a pivotal link to explain progressive collagen degeneration and osteoarthritic changes. In human medicine, recent reports have identified relaxin as a triggering factor in ligament ruptures in knee and metacarpal joints. We thus hypothesized that relaxin might also play a role in canine cruciate ligament rupture. Relaxin’s primarily known property is connective tissue remodeling through collagenolysis. We therefore investigated relaxin and its cognate receptors LGR7/LGR8 in 18 dogs with cranial cruciate ligament disease (CCLD) and compared them to a group of dogs with normal stifle joints. Applying immunohistochemistry (IHC), double immunofluorescence (dIF), and western blot analysis (WB), we found strong and significantly increased expression of both relaxin and its receptors in ruptured cruciate ligaments, and in synovial membranes. Pattern of immuno-staining on dIF strongly suggests relaxin binding to primed receptors and activation of signaling properties, which in turn may have affected collagen matrix metabolism. Thus, in canine cranial cruciate ligament disease, relaxin/receptor signaling may be a primary trigger for collagen fiber degradation and collagen lysis, eventually followed by ligament rupture.

Chronic non-septic pleural effusion is a condition that frequently may occur because of lung or pleural neoplasia, or chylothorax refractory to surgical treatment, in dogs. Effusion management can be performed with multiple pleurocenteses or the application of chest drains. New modified vascular devices have been used for patients with chronic diseases; they offer the advantage of allowing home management and do not require hospitalization. Eight PleuralPort^TM devices were applied in seven dogs during thoracoscopic exploration and biopsy procedures; five were affected by mesothelioma; one by lung metastases from a mammary carcinoma; and one by chronic chylothorax. The median time of surgical procedure was 51 min; one developed pneumothorax post-operatively that resolved within 12 h after repeated drainage; one device was obstructed after 45 days and was successfully managed by flushing. All patients were discharged after 24 h. The median duration of port insertion in cancer patients was 5 months and those dogs were euthanized because of tumor progression; in the dog with chylothorax, the device was removed after 1 year when the effusion had resolved.

(1) Background: Postoperative antibiotic prophylaxis in dogs undergoing tibial plateau leveling osteotomy (TPLO) is controversial. We evaluated the effect of perioperative antibiotic administration on the incidence of surgical site infection (SSI) and bone healing in dogs that underwent TPLO procedures and compared this protocol with cases that received prolonged postoperative antibiotic treatment. (2) Methods: Two different antibiotic treatment protocols were used. In group A, cefazolin (22 mg/kg IV) was administered preoperatively 30–60 min before skin incision and repeated every 90–120 min intraoperatively. Antimicrobial prophylaxis was extended in the postoperative period with oral cefazolin (22 mg/kg BID) for 10 days after surgery. In group B, dogs only received perioperative treatment, at the same dose used in group A. Dogs were considered to have SSI in cases of incisional drainage, wound dehiscence, positive bacterial culture, or evidence of radiographic signs of infection. (3) Results: In group A, SSI was observed in 3/61 TPLOs (4.9%). In group B, SSI was present in 3/51 TPLOs (5.9%). There was no difference between the two groups. (4) Conclusions: Our results indicate that perioperative antibiotic prophylaxis in TPLO procedures is sufficient to maintain overall low rates of SSI. The incidence of SSI was similarly low compared to the rate observed in dogs that also received postoperative antibiotic treatment.