“Phossy jaw,” a disfiguring ailment of the 19th century, was once a grim reality for workers in early match factories. This occupational disease, caused by exposure to white phosphorus, led to severe jawbone decay. While the classic industrial form has been virtually eliminated through public health efforts and global bans, a strikingly similar condition affecting the jawbone can arise today from entirely different sources.
The Historical Disease
The historical “phossy jaw,” formally known as phosphorus necrosis of the jaw, originated from extensive exposure to white phosphorus, a highly reactive and toxic substance used in “strike-anywhere” matches. Workers in poorly ventilated factories often inhaled phosphorus vapors or ingested particles, leading to a slow, debilitating poisoning. Over time, this exposure caused the jawbone to die and separate from living tissue, a process known as necrosis.
The disease manifested with unbearable abscesses, persistent pain, and eventual loss of teeth, often resulting in severe facial disfigurement and, in some cases, fatal complications. The plight of these workers, highlighted by events like the London matchgirls’ strike in 1888, galvanized public outcry. This led to international agreements and legislation, culminating in bans on white phosphorus in match production by the early 20th century, prompting the widespread adoption of safer red phosphorus.
Modern Parallels and Causes
Today, the most common condition resembling “phossy jaw” is Medication-Related Osteonecrosis of the Jaw (MRONJ). This condition primarily arises as a rare side effect of certain medications, particularly a class of drugs called bisphosphonates. These drugs are widely prescribed to treat conditions that weaken bones, such as osteoporosis, and to manage bone complications in cancer patients. Bisphosphonates work by inhibiting osteoclasts, cells that break down bone, thereby strengthening the skeletal structure.
Despite their benefits, these medications can interfere with the natural healing process of the jawbone, particularly after dental procedures like tooth extractions, or sometimes even spontaneously. The risk of MRONJ is low for patients taking oral bisphosphonates for osteoporosis, but considerably higher for cancer patients receiving higher doses of intravenous bisphosphonates. Other medications like denosumab and antiangiogenic agents, used in cancer treatment, also pose a risk for MRONJ.
Beyond medication, direct exposure to white phosphorus, though exceedingly rare in modern contexts, can still cause osteonecrosis of the jaw. This might occur in specialized situations, such as the illicit manufacturing of fireworks or in military scenarios involving certain chemical weapons. These instances represent a direct, albeit uncommon, link to the original historical cause of “phossy jaw.”
Symptoms and Treatment in the Modern Era
Symptoms of modern jawbone necrosis, particularly MRONJ, often include persistent pain in the jaw, swelling, and the loosening of teeth. Patients may also experience a foul-smelling discharge from the gums or jaw, difficulty fully opening their mouth, and altered sensations like numbness or tingling. A distinguishing sign is the visible exposure of necrotic bone through the gum tissue, which can persist for over eight weeks. The lower jaw is more frequently affected than the upper jaw, partly due to its comparatively reduced blood supply.
The management of MRONJ in the modern era typically involves a conservative approach, focusing on controlling infection and pain. Treatment often includes the use of systemic antibiotics, along with antibacterial mouth rinses, such as chlorhexidine. Minor surgical procedures, known as debridement or sequestrectomy, may be performed to carefully remove the exposed dead bone fragments. This modern, targeted treatment contrasts sharply with the historical approach, which often necessitated extensive and disfiguring surgical removal of the jawbone.