The Biology of Locking Plate Applications

Changes in tibial cortical dimensions and density associated with long‐term locking plate fixation in goats

“…The definitive etiology of cortical porosis following compression plate fixation remains unclear [20]. Proposed etiologies include stress‐shielding of the bone leading to disuse resorption or disruption of cortical perfusion either by surgical trauma or compression between the plate and periosteum [29, 49]. However, plate alterations aimed at reducing plate contact (e.g., limited contact dynamic compression plate) and/or stress differential between plate and bone (e.g., plate material compositions) have not succeeded in eliminating porosis and reducing refracture rates [3, 20, 21, 48].…”

“…In theory, the differing contact profiles and fixation biomechanics between locking and compression plate fixation should reduce the incidence of cis‐cortical porosis following locking plate fixation. However, Moens describes several clinical case series and studies that found no difference in cortical necrosis or porosity between locking and compressive plates [29]. Also, progressive bone atrophy (characterized by cortical thinning and porosis) following locking plate fixation of diaphyseal forearm fractures has been reported [18, 25, 32].…”

“…Also, progressive bone atrophy (characterized by cortical thinning and porosis) following locking plate fixation of diaphyseal forearm fractures has been reported [18, 25, 32]. Moens challenged the claim that locking plates do not induce cortical porosis, citing a lack of in depth and rigorous comparisons between traditional compression and locking plates [29].…”

“…Landmark achievements include the development of metallic alloys for orthopedic plates, the establishment of the Arbeitgemeinschaft fur Osteosynthesefragen (AO) principles of effective fracture treatment, the invention of compression plates to encourage primary bone healing of fractures, the refinement of plate hole designs to allow for tension or dynamic compression plating, and the establishment of minimally invasive plate osteosynthesis [1, 40, 49]. Fixed angle devices, such as point‐contact fixators and locking plates, were developed to respond to the challenges observed during conventional compression plating including marked soft tissue and periosteal damage during fixation, stress shielding of the underlying bone, and complications such as cortical porosis and/or refracture following plate removal [1, 12, 20, 29, 45].…”

“…Initially described as a cancellous transformation of cortical bone under the plate, cortical porosis represents a structural change to bone in contact with the plate characterized by bone resorption, medullary widening, and cortical thinning [31]. This comorbidity has been associated with increased refracture rates following plate removal and poses a challenge to clinicians who must balance radiographic fracture healing with increasing cortical porosity risk in their plate removal decisions [29, 48]. The definitive etiology of cortical porosis following compression plate fixation remains unclear [20].…”