Something was wrong with Whiskey, and it wasn’t lethargy, whining or refusal to eat that tipped off his owners. It was chew sticks, unchewed. For the 10-year-old Small Munsterlander, chewing was a lifelong obsession. It had been a good life, one spent running down San Francisco city sidewalks; playing in the parks; exploring neighborhood shops; and, of course, chasing toys on the beach.
Whiskey’s owners, Tom Swierk and Robin Addams, indulged his appetite for beef tendons and other treats. The dog they had acquired as a young pup still had “lots of sass,” as Swierk describes him, or he did until last Thanksgiving, when his owners realized he had lost interest in chewing, one of his favorite pastimes. The Small Munsterlander, a hunting breed that originated in Munster, Germany, has been bred for centuries to thrive on chasing and retrieving. True to his roots, Whiskey was a friendly, devoted dog with an intense streak that his owners channeled into play. When Whisky ignored his chew toys, Swierk thought it was a problem with a tooth, and took him to the vet.
It was cancer.
Oral cancer, both malignant and benign, is not uncommon in dogs. Unfortunately, Whiskey’s tumor wasn’t benign. The lesion on his lower left gum was malignant squamous cell carcinoma, the second most common oral malignancy in dogs. In humans, it accounts for 70 percent of all oral tumors.
The wrenching news came with a silver lining: the cancer hadn’t spread to other organs. “This type of malignant tumor metastasizes less than 10 percent of the time,” Swierk says. It is known for its aggressive growth, however, and the tumor had already invaded Whiskey’s jawbone. Nearby were lymph nodes, a ready target and a pathway for the cancer to spread.
What, then, could be done? The usual course of action was to amputate the affected bone, sometimes using chemotherapy and radiation. Another common treatment involved shaving the growth, Swierk says, but that would also mean subsequent periodic surgeries. With the diseased bone removed, Whiskey’s chances for a full recovery were good. A life without chewing, however, wasn’t so promising.
After amputation, the jaw is never quite the same. The teeth and bones gradually fall out of alignment, and the dog’s teeth can cause ulcerations in the hard palate. He could eat, but there would be no more chew toys. He could not play ball or tug of war.
As it turned out, there was another option. A team of vets at the University of California, Davis, had been working on a fix for pets who lost jawbone to disease or injury. It had only been used in five other dogs, but the results had been good. Their vet referred him to the UC Davis School of Veterinary Medicine, 73 miles east of San Francisco.
It was a done deal for Swierk and Addams, who were prepared to travel to New York, if that’s what it took to not only save their dog, but have him back whole, and to pay the $8,000 treatment cost. Whiskey was more than a pet to them — he was their companion.
“Whiskey is our world, plain and simple,” Swierk says.
Bone regeneration was seen as science fiction in 1948, when Dr. Marshall R. Urist, a UCLA orthopedic surgeon who pioneered the field, got started. Urist spent five decades at the bone research laboratory at UCLA, where he discovered how to use proteins to stimulate skeletal repair.
In 1971, he proposed the name “bone morphogenetic protein” (BMP) for the growth-promoting factors he used to prompt new bone growth in rabbits. The bone proteins act as signals to stem cells, which migrate to them and are converted into bone-forming cells. These cells then grow bone in the area where the BMP was placed.
Naturally occurring BMP is found within bone, but clinically useful amounts can’t be easily extracted from human donor bone and so must be genetically engineered in the lab.