The sensitivity of phosphofructokinase to stimulation by sulfate, adenosine monophosphate, and cyclic adenosine monophosphate is decreased in otosclerosis. The enzyme is unresponsive to inhibition by a citrate and markedly stimulated by lactate, normally not an effector.
The evidence suggests that aberrant phosphofructokinase is operative in otosclerosis. This would cause defective regulation of glycolysis and a consequent imbalance between the anaerobic and aerobic phases of metabolism. Evidence from this and other studies supports the conclusion that otosclerotic bone is abnormally geared to a primarily aerobic metabolism.