Neuropathic osteoarthropathy presents the most dramatic radiographic picture of all of the arthropathies. As a result, it may produce a diagnostic dilemma. Although it is known that various neurological disorders play a prominent role in the development of the osteoarthropathy, the exact pathogenesis has not been clearly established. Although chronic, repetitive, and undetected trauma creates many of the radiographic changes, it is not responsible for all of the changes seen. As long as trauma is believed to be the primary etiology, many neuropathic joints will continue to be misdiagnosed as infection or tumor.
The radiographic changes in neuropathic osteoarthropathy cover the complete spectrum of bone change from total resorption to excessive repair. At one end of the spectrum is the hypertrophic joint and at the other end is the atrophic joint. Each of these extremes is discussed separately.
The hypertrophic joint
The hypertrophic joint, or bone productive joint, if put in a time sequence, should be called the “chronic joint.” The radiographic changes present no diagnostic problem. The changes resemble osteoarthritis “with a vengeance.” The hallmarks are the following:
- 1.
Dissolution of normal joint articulation
- 2.
Severe subluxation or dislocation
- 3.
Excessive juxta-articular new bone formation
- 4.
Mammoth osteophytes
- 5.
Fragmentation and osseous debris
- 6.
Pathological fractures
- 7.
Unilateral or bilateral asymmetrical involvement
- 8.
Distribution in weight-bearing joints (i.e., foot, ankle, knee, hip, spine)
The Foot and Ankle
Diabetes mellitus is the most common cause of neuropathic osteoarthropathy even though it occurs in only 5 to 10 percent of patients with diabetes. In patients who are diabetic, the forefoot and midfoot are the most commonly involved joints. However, in diabetes, infection is commonly present, and it becomes difficult to separate neuropathic changes from those of chronic osteomyelitis. The most common neuropathic change seen in the foot is radiographic evidence of a longstanding Lisfranc fracture-dislocation with extensive eburnation and fragmentation around the tarsometatarsal joints ( Fig. 14-1 ). Bizarre fractures of the calcaneus with dissolution of the talocalcaneal joint and tumbling of the talus into the calcaneus may be the neuropathic change ( Fig. 14-2 ). In the ankle, the distal fibula may fracture pathologically and the talus may angulate within the ankle mortise. With time, massive bone sclerosis, osteophytosis, and osseous debris develop ( Fig. 14-3 ).
Knee and Hip
These joints are most commonly involved in tabes dorsalis. Sixty to 70 percent of patients with this condition have lower extremity involvement. In the knee, the first radiographic change is recurrent massive effusion with some subluxation. Periarticular pathological fractures and bone debris within the joint may develop ( Fig. 14-4 ). Eventually, with weight bearing, there is joint dissolution, subluxation, eburnation, and fragmentation ( Fig. 14-5 ).
Early resorptive changes in the hip may or may not be seen prior to the hypertrophic changes. As long as the patient is weight bearing, productive bone changes develop around the femoral head, and a pseudoacetabulum is formed where the head has subluxed from the normal acetabulum ( Fig. 14-6 ).
