Understanding The Potential Impact Of Diabetes On Bone Biology And Biomechanics
Cancellous (trabecular) bone has approximately 20 times more surface area per unit volume than cortical bone. It also has about 50 to 90 percent porosity, which gives it a much higher rate of metabolic activity because of greater accessibility to adjacent cellular constituents.
In long bones, there is a biomechanical interplay that takes place between the cortical and cancellous bone. This interplay may have greater consequences for the insensate diabetic patient.
In long bones, the diaphyseal cortical regions will resist torsion and bending forces. Where the cortical bone thins out at the neck of the bone (the “cutback region”), it has the support of the underlying epiphyseal-metaphyseal cancellous bone. This allows for greater deformation under equal loads. This unique complex formed by articular cartilage, cancellous bone and cortical bone acts to absorb impact loads. Replacement of this complex by a joint prosthesis may eliminate shock absorption with resultant increased peak loads to the diaphyseal cortical bone.
Cortical or cancellous bone may consist of woven (primary) or lamellar (secondary) bone. Woven bone consists of irregular and random oriented collagen fibrils. It is isotropic, meaning that it responds the same no matter the direction of applied forces. It is rarely present after the age of 4 with the exception of pathologic processes.
Lamellar bone consists of densely packed, well-organized collagen fibrils. It is anisotropic as its mechanical properties will differ based on the direction of applied forces.
Osteons form the bulk of the diaphyseal cortex. They are composed of irregular, anastomosing and longitudinal cylinders formed from concentric lamellae. This longitudinal orientation explains why long bones resist coaxial forces much better than perpendicular forces. Haversian canals form the central conduit of the osteon. These canals are connected to one another via canaliculi. Cement lines define and separate each individual osteonal complex. Canaliculi and collagen fibrils will not cross cement lines. For this reason, cracks will follow cement lines rather than cross osteons.
When treating the diabetic patient for either trauma or for elective reconstruction, one must take into account the various factors that may impede normal bone healing. These factors may include poor long-term blood glucose control, poor nutritional status, poor vascularity and long-term osteodystrophy.
In order to balance these deleterious factors, one should consider utilizing more aggressive fixation constructs, surgical strategies that yield little soft tissue compromise, tuning up nutritional factors and incorporating modern orthobiologic materials and techniques.
Dr. Weinraub is a Fellow of the American College of Foot and Ankle Surgeons. He is a Clinical Assistant Professor of Medicine at the University of Virginia and a Clinical Assistant Professor of Orthopaedic and Podiatric Surgery at the Virginia College of Osteopathic Medicine. Dr. Weinraub can be contacted at email@example.com.
Dr. Steinberg (pictured) is an Assistant Professor in the Department of Surgery at the Georgetown University School of Medicine in Washington, D.C. He is a Fellow of the American College of Foot and Ankle Surgeons.
1. Perren SM. Physical and biological aspects of fracture healing with special reference to internal fixation. Clin Orthopaedics and Related Research. 138: 175-195, 1979.
2. Macey LR, Kana SM, Jingushi S, Terek RM, Borretos J, Bolander ME. Defects of early fracture healing in experimental diabetes. J Bone Joint Surg Am, 71 (5), 722-733, 1989.
3. Funk JR, Hale JE, Carmines D, Gooch HL, Hurwitz SR. Biomechanical evaluation of early fracture healing in normal and diabetic rats. J Orthop Res. 18 (1), 126-132, 2000.
4. Boddenberg U. Healing time of foot and ankle fractures in patients with diabetes mellitus: literature review and report of own cases. Zentralbl Chir. 129 (6), 453-459, 2004.
5. Kloting N, Follak N, Kloting I. Is there an autoimmune process in bone? Gene expression studies in diabetic and nondiabetic BB rats as well as BB rat related and unrelated rat strains. Physiol Genomics, 24 (1), 59-64, 2005.