Subtotal or partial unilateral arytenoidectomy for treatment of arytenoid chondritis in five calves.

CASE DESCRIPTION: 5 calves were evaluated for abnormal respiratory noise associated with variable degrees of respiratory distress. CLINICAL FINDINGS: Tachypnea and inspiratory dyspnea were detected at initial evaluation in all calves. Endoscopic evaluation of the upper respiratory tract revealed enlarged and immobile arytenoids. Radiographic (n = 3) and computed tomographic (1) evaluation of the laryngeal area revealed images that were indicative of a large soft tissue mass at the level of the arytenoids obstructing the rima glottis. A presumptive diagnosis of arytenoid chondritis was made. TREATMENT AND OUTCOME: A tracheostomy tube was placed in all calves. Medical treatment (with antimicrobials and anti-inflammatory drugs) was attempted in 4 calves after initial evaluation. Unilateral arytenoidectomy via a laryngotomy was performed under general anesthesia in all calves. Dysphagia and coughing were the most frequent postoperative complications. Three calves survived at least 6 months after the procedure. One calf died of a perforated abomasal ulcer 3 months after the surgery. Another calf died suddenly 1 month after the surgery of an undetermined cause. CLINICAL RELEVANCE: Unilateral arytenoidectomy was a viable surgical treatment for arytenoid chondritis in calves. Further research in a larger number of affected cattle is needed to determine the advantages or disadvantages of this procedure over other surgical techniques.

Spontaneous calcification of arteries and cartilage in mice lacking matrix GLA protein.

Calcification of the extracellular matrix (ECM) can be physiological or pathological. Physiological calcification occurs in bone when the soft ECM is converted into a rigid material capable of sustaining mechanical force; pathological calcification can occur in arteries and cartilage and other soft tissues. No molecular determinant regulating ECM calcification has yet been identified. A candidate molecule is matrix GLA protein (Mgp), a mineral-binding ECM protein synthesized by vascular smooth-muscle cells and chondrocytes, two cell types that produce an uncalcified ECM. Mice that lack Mgp develop to term but die within two months as a result of arterial calcification which leads to blood-vessel rupture. Chondrocytes that elaborate a typical cartilage matrix can be seen in the affected arteries. Mgp-deficient mice additionally exhibit inappropriate calcification of various cartilages, including the growth plate, which eventually leads to short stature, osteopenia and fractures. These results indicate that ECM calcification must be actively inhibited in soft tissues. To our knowledge, Mgp is the first inhibitor of calcification of arteries and cartilage to be characterized in vivo.