Understanding The Potential Impact Of Diabetes On Bone Biology And Biomechanics
It is well established that poorly controlled diabetes mellitus leads to vasculopathy, immunopathy and neuropathy, all of which may contribute to osteopathy. However, in order to understand the nuances of bone healing in the diabetic population, one must first have a strong grasp of the fundamentals of bone biology and biomechanics (see “A Helpful Primer On Bone Structure” below).
Bone is a dynamic medium with a multifactorial purpose including support of soft tissues, protection of soft tissues, locomotion and being a mineral reservoir. The growth, maintenance and healing of bone requires its formation throughout one’s life. In fact, the rate of bone turnover approaches 100 percent in the first year of life but declines to an approximate 10 percent turnover rate during adolescence.
Bone has a tensile strength that is almost equal to that of cast iron yet is 10 times more flexible. Bone constantly changes in response to hormonal and mechanical signals. Seemingly dissimilar conditions such as embryonic development, bone growth, bone remodeling, fracture healing and arthrodesis all rely on the same basic premise that mesenchymal stem cells functioning in a vascular environment will become normal osteoblasts that secrete a specialized extracellular matrix. This matrix will mineralize and the osteoblasts trapped within the mineralized matrix will become osteocytes. This will be followed by osteoclasts, which herald the remodeling process to convert immature woven bone into mature lamellar bone, and to resorb and replace mature lamellar bone.
Although there is only one real mechanism for bone formation, it may occur within a cartilage precursor (enchondral bone formation), an organic matrix membrane (intramembranous bone formation) or via the deposition of new bone on pre-existing bone (appositional bone formation).
A Pertinent Overview Of Bone Healing
There are over 6.2 million fractures per year in the United States. These fractures will generally heal either via secondary (enchondral) or primary (direct or intramembranous) bone healing. The route of bone formation is contingent upon the degree of interfragmentary stability.
Perren’s theory of strain states there is a relationship between decreasing strain and increasing the potential for osteogenesis across a fracture or fusion site.1 According to Perren’s theory of strain, when there are two given fracture segments, the healing interface will have force generated motion potential that is contingent upon the stability of the original fixation construct.
Mathematically, strain is equal to the change in the interface length divided by the original interface length for any given force. Therefore, with an unstable construct, the healing gap may undergo excessive motion with resultant increasing strain. Researchers have shown that strain of less than 2 percent will yield absolute stability and subsequent primary bone healing.
One sees primary bone healing with compression screw fixation because of the great friction generated between the healing segments. Unfortunately, if the compression fails, there may be significant increased motion and subsequent strain. If strain exceeds 10 percent, there is a high likelihood of fibrous non-union. If strain resides between 2 to 10 percent, there will be micromotion with subsequent callus formation and secondary bone healing.
Does Diabetes Delay Bone Healing?
Now, how does diabetes affect bone healing scenarios?
A study by Macey, et. al., tested the hypothesis that untreated diabetes mellitus would result in impaired fracture healing.2 This animal study used femora of normal rats and from untreated and insulin treated diabetic rats. Researchers created a closed femoral fracture in each rat population. When evaluating bone healing in the untreated diabetic rat population, they noted a 29 percent decrease in tensile strength and a 50 percent decrease in stiffness compared to the controls.