Phosphorus jaw, known as phosphorus necrosis of the jaw, was a severe occupational disease primarily affecting the jawbone. It emerged as a serious public health concern in the 19th and early 20th centuries, linked directly to specific industrial practices. Modern occupational health measures have eliminated the working conditions that led to this disease.
The Historical Context of Phossy Jaw
The disease emerged in the 19th century, particularly in the matchstick industry. The production of “strike-anywhere” matches relied on white phosphorus for ignition. Workers, often young women and girls, were exposed to toxic fumes through inhalation and skin contact. Poor ventilation and long shifts, sometimes 10-15 hours daily, exacerbated their exposure as they dipped wooden splints into heated phosphorus mixtures.
The first case of phosphorus jaw was diagnosed in 1839 in Vienna, affecting a female matchstick maker exposed for five years. Hundreds of workers, often from impoverished backgrounds, developed this condition. The plight of these “matchgirls” gained public attention through social activist Annie Besant, who published an article in The Link in 1888. This exposé detailed the meager wages, punitive fines, and hazardous conditions at factories like Bryant & May in London, leading to the historic Matchgirls’ Strike of 1888.
The strike did not immediately ban white phosphorus use, but it drew significant attention to the dangers. Safer alternatives existed, such as the less toxic red phosphorus, which was more stable and less reactive. Despite the availability of red phosphorus, manufacturers often favored the cheaper white phosphorus. International agreements, like the Berne Convention of 1906, eventually led to a worldwide ban on white phosphorus in match production, with a total ban in Britain by 1910, effectively eradicating the historical disease.
Signs and Symptoms
Individuals with phosphorus jaw experienced a progressive series of symptoms. The condition began with persistent toothaches and noticeable swelling of the gums. As the disease advanced, pus-filled abscesses would form, sometimes leading to fistulas, which are abnormal passages that penetrate the oral mucosa. This progression frequently resulted in the loosening and eventual loss of teeth.
A characteristic of the disease was the eventual death of the jawbone, known as osteonecrosis. Within three to six months of symptom onset, dead bone, or sequestrum, would separate from the living bone, often appearing porous. The decaying bone tissue would emit a foul-smelling discharge and, in some reported cases, even glowed with a greenish-white phosphorescent light in darkened rooms. While the lower jaw was more commonly affected, the upper jaw could also be involved, sometimes leading to the spread of abscesses to the eye socket.
Modern Parallels and Causes
While historical phosphorus jaw has been eradicated, a related condition exists today: medication-related osteonecrosis of the jaw (MRONJ). This modern form is not caused by industrial chemical exposure but by certain medications, most notably bisphosphonates. These drugs are widely prescribed to treat conditions involving excessive bone breakdown, such as osteoporosis, multiple myeloma, and bone metastases associated with various cancers.
Bisphosphonates work by inhibiting the activity of osteoclasts, cells responsible for bone resorption. By slowing this process, the drugs help strengthen bone and reduce fracture risk. However, in rare instances, particularly with high doses or prolonged use, these medications can disrupt the jawbone’s natural repair mechanisms and blood supply. This impairment in bone turnover and healing capacity can lead to localized bone death, especially in areas of the jaw subjected to trauma, such as after tooth extractions.
Other medications beyond bisphosphonates have also been linked to MRONJ, including denosumab, another antiresorptive agent, and certain anti-angiogenic drugs used in cancer treatment. Anti-angiogenic drugs inhibit the formation of new blood vessels, which can contribute to osteonecrosis by depriving bone tissue of adequate blood supply. While exact mechanisms are still being researched, the common thread is a disruption of the jawbone’s ability to repair and maintain itself, leading to exposed, non-healing bone.
Diagnosis and Management
Diagnosing medication-related osteonecrosis of the jaw (MRONJ) involves clinical assessment, patient history, and imaging studies. Doctors look for exposed bone in the maxillofacial region that has persisted for more than eight weeks in patients who have received antiresorptive or anti-angiogenic medications and have no history of radiation to the jaw. A thorough oral examination and a detailed review of the patient’s medication history provide important diagnostic clues.
Imaging techniques such as dental X-rays and CT scans help assess the extent of bone involvement and rule out other conditions. These images can reveal characteristic changes in the jawbones, such as areas of sclerosis or the presence of sequestra. Early detection is important, and patients on these medications are advised to maintain good oral hygiene and undergo regular dental check-ups to minimize risk.
Current management strategies for MRONJ are conservative, aiming to alleviate symptoms and prevent further progression. This includes antibiotics to control infection, antibacterial mouth rinses, and pain management. In cases where conservative measures are insufficient or the condition is more advanced, minor surgical procedures, such as debridement to remove dead bone, may be performed. This contrasts sharply with the historical approach to phosphorus jaw, which involved drastic surgical removal of significant portions or even the entire jawbone, leading to severe disfigurement and difficulty eating.