In school, we learned to be suspicious of a bone stress injury (BSI) if there was pinpointed tenderness on a bone along with pain when loading the limb. This is typically on point with more superficial locations of bone injury in the lower limb, but doesn’t really prepare us to suspect BSI in more proximal locations like the hip, thigh or pelvis where symptoms are less straightforward. 

 

Pain presentation varies widely with bone stress injuries, with descriptions ranging from a tightness or stiffness to a dull ache to sharp local pain, or a combination of those descriptors. This variance is in part due to the innervation or nerve supply of bone, and the sensitivity of different regions of bone to mechanical and chemical stimuli. 

 

Bone is innervated by two types of sensory nerve fibers, both of which are sensitive and respond to mechanical and chemical signals. Mechanical signals result from loading, such as putting weight on your leg. In an injured bone, the mechanical or structural integrity may be compromised to the point that tension or compression result in pain. Chemical signals come from the body’s own processes - in the case of a bone injury, inflammatory chemicals sent to the area to start the repair process stimulate the nerve fibers and cause pain. Without these sensory fibers sending signals to the brain, we don’t have pain - which sounds cool at first, but if we didn’t have pain signals we’d be at risk for even further damage. 

 

The relative density of these sensory fibers varies between parts of bone: the ratio is 100:2:0.1 in the outer bone covering (periosteum), bone marrow and cortical bone, respectively. Notice how much that relative density differs - no wonder pain presentation is so different from one bone injury to the next. 

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Bone injuries that involve regions with a higher density of sensory fibers like the periosteal surface (lining of the bone) lead to more localized and sharper pain. Injuries in regions such as the bone marrow cavity or trabecular bone result in more vague and diffuse pain because of the lower density of sensory fibers as well as the deeper location.

 

It’s thought that the initial pain from a stress reaction (early to mid-stage on bone stress injury spectrum - see this blog for more details on stages) comes from the stimulation of sensory fibers by inflammatory chemicals. This is why some bone stress injuries won’t initially present with consistent pain with loading activities like running or jumping - the mechanical structure of the bone is still intact, so pain is primarily resulting from that inflammatory response. This is a GREAT time to catch a BSI early to avoid negative consequences of delayed treatment or healing.

 

Once symptoms have progressed to being present during bone-loading activities, the bone’s mechanical properties have been compromised - this is usually when runners seek treatment as the pain is now starting to impact their training. During loading, the concentration of stressors at the injured site stretches the periosteum, or the bone lining, and increases pressure inside the bone marrow cavity. Since the periosteum has a high density of sensory fibers, the stretching often causes sharp, local pain; the increased pressure in the marrow cavity leads to more diffuse, aching pain because of the lower density of sensory fibers there. Once the load is removed or once someone is resting, that sharp stretching pain goes away, but the increase in pressure remains, contributing to a continued ache at rest and often at night.