The advent of 'biological internal fixation' is an important development in the surgical management of fractures. Locked nailing has demonstrated that flexible fixation without precise reduction results in reliable healing. While external fixators are mainly used today to provide temporary fixation in fractures after severe injury, the internal fixator offers flexible fixation, maintaining the advantages of the external fixator but allowing long-term treatment. The internal fixator resembles a plate but functions differently. It is based on pure splinting rather than compression. The resulting flexible stabilisation induces the formation of callus. With the use of locked threaded bolts, the application of the internal fixator foregoes the need of adaptation of the shape of the splint to that of the bone during surgery. Thus, it is possible to apply the internal fixator as a minimally invasive percutaneous osteosynthesis (MIPO). Minimal surgical trauma and flexible fixation allow prompt healing when the blood supply to bone is maintained or can be restored early. The scientific basis of the fixation and function of these new implants has been reviewed. The biomechanical aspects principally address the degree of instability which may be tolerated by fracture healing under different biological conditions. Fractures may heal spontaneously in spite of gross instability while minimal, even non-visible, instability may be deleterious for rigidly fixed small fracture gaps. The theory of strain offers an explanation for the maximum instability which will be tolerated and the minimal degree required for induction of callus formation. The biological aspects of damage to the blood supply, necrosis and temporary porosity explain the importance of avoiding extensive contact of the implant with bone. The phenomenon of bone loss and stress protection has a biological rather than a mechanical explanation. The same mechanism of necrosis-induced internal remodelling may explain the basic process of direct healing.

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The tissue response and in vivo molecular stability of injection-molded polyhydroxyacids--polylactides (PLA), poly(3-hydroxybutyrate) (PHB), and poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHB/VA, 5-22% VA content)--were studied. Polymers were implanted subcutaneously in mice and extirpated at 1, 3, and 6 months in order to study tissue response and polymer degradation. All polymers were well tolerated by the tissue. No acute inflammation, abscess formation, or tissue necrosis was observed in tissues adjacent to the implanted materials. Furthermore, no tissue reactivity or cellular mobilization was evident remote from the implant site. Mononuclear macrophages, proliferating fibroblasts, and mature vascularized fibrous capsules were typical of the tissue response. Degradation of the polymers was accompanied by an increase in collagen deposition. For the polylactide series, the inflammatory response after 1 month of implantation was less for materials containing the D-unit in the polymer chain, whereas in the case of the polyhydroxybutyrate/valerates, the number of inflammatory cells increased with increasing content of the valerate unit in the polymer chain. Between 1-3 months, there was slightly more tissue response to the PHB and PHB/VA polymers than to PLA. This response is attributed to the presence of leachable impurities and a low molecular weight soluble component in the polyhydroxybutyrate/valerates. At 6 months, the extent of tissue reaction was similar for both types of polymers. All polylactides degraded significantly (56-99%) by 6 months. For a poly(L-lactide) series, degradation rate in vivo decreased with increasing initial molecular weight of the injection-molded polymer. Several samples showed pronounced bimodal molecular weight distributions (MWD), which may be due to differences in degradation rate, resulting from variability in distribution of crystalline and amorphous regions within the samples. This may also be the result of two different mechanisms, i.e., nonenzymatic and enzymatic, which are involved in the degradation process, the latter being more extensive at the later stage of partially hydrolyzed polymer. The PHB and PHB/VA polymers degraded less (15-43%) than the polylactides following 6 months of implantation. Generally, the polymer with higher valerate content (19%, 22%) degraded most. The decrease in molecular weight was accompanied by a narrowing of the MWD for PHB and copolymers; there was no evidence of a bimodal MWD, possibly indicating that the critical molecular weight that would permit enzyme/polymer interaction had not been reached. Weight loss during implantation ranged from 0-50% for the polylactides, whereas for the PHB polymers weight loss ranged from 0-1.6%.

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