A unified theory of bone healing and nonunion

Abstract

This article presents a unified clinical theory that links established facts about the physiology of bone and homeostasis, with those involved in the healing of fractures and the development of nonunion. The key to this theory is the concept that the tissue that forms in and around a fracture should be considered a specific functional entity. This 'bone-healing unit' produces a physiological response to its biological and mechanical environment, which leads to the normal healing of bone. This tissue responds to mechanical forces and functions according to Wolff's law, Perren's strain theory and Frost's concept of the "mechanostat". In response to the local mechanical environment, the bone-healing unit normally changes with time, producing different tissues that can tolerate various levels of strain. The normal result is the formation of bone that bridges the fracture - healing by callus. Nonunion occurs when the bone-healing unit fails either due to mechanical or biological problems or a combination of both. In clinical practice, the majority of nonunions are due to mechanical problems with instability, resulting in too much strain at the fracture site. In most nonunions, there is an intact bone-healing unit. We suggest that this maintains its biological potential to heal, but fails to function due to the mechanical conditions. The theory predicts the healing pattern of multifragmentary fractures and the observed morphological characteristics of different nonunions. It suggests that the majority of nonunions will heal if the correct mechanical environment is produced by surgery, without the need for biological adjuncts such as autologous bone graft. Cite this article: Bone Joint J 2016;98-B:884-91.

Bone fracture healing in mechanobiological modeling: A review of principles and methods

“…In BHN, the bone is in homeostatsis when under tolerable strain (much less than 2%). For strains greater than 2% and less than 100%, a fracture occurs and is considered to be the beginning of the “bone-healing organ.” Finally, for strains above 100%, the “bone-healing organ” stops and fails to heal, leading to nonunion (Elliott et al, 2016).

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Gelatin Nanoparticle‐Injectable Platelet‐Rich Fibrin Double Network Hydrogels with Local Adaptability and Bioactivity for Enhanced Osteogenesis

“…After the finite element calculation, the strain maps of the above three groups were obtained. According to Wolff's law, all bone filling materials are influenced by the external strain, to which bone tissues will respond . The unit from bone tissues that responds to mechanical environment and generates a physiological response is defined as “bone healing unit.” The microstrain from 50 to 3000 µε of bone healing unit is beneficial for bone healing process .…”

Kırık iyileşmesi

“…Kırık iyileşmesi ile ilgili pek çok teori ortaya atılmıştır; bunlardan bazıları Şekil 6 a-d'de grafiklerle teorik olarak açıklanmaya çalışılmıştır. [30][31][32][33][34] Perren'in araştırma sonuçları, dinamik deformasyon yokluğunun kallus oluşumunun mekanik indüksiyonunun da eksikliğine yol açtığı, çok küçük oranlarda gerinimin kallus oluşumunu tetiklediği şeklindedir. Perren'in fragmanlar arası gerinim teorisine göre, %2'ye kadar gerinim lamellar kemik tarafından tolere edilirken, gerinim %10'a kadar ise immatür (woven) kemik bunu iyi tolere edebilir, ancak bunun üzerinde (%10-30) ise rezorpsiyon ortaya çı-kacaktır.…”

“…ise, tüm kırığı, fonksiyonel bir ünite olarak çalışan ve biyolojik ve mekanik stimulusa yanıt veren bir "kemikle iyileşen organ" olarak düşünmek-tedir. [33] Araştırmacı; Wolff kanunu (normal kemiğin mekanik çevreye yanıtı); Perren gerinim teorisi (kırık kemiğin mekanik çevreye yanıtı) ve Frost "mekanostat" modelini (mekanik çevreye kemik hemostaz yanıtı) Kemik yüklendiğinde kırık fragmanlar yer değiştirir; bu hareket kırık hattında çok yönlü farklı kuvvetlerin (aksiyel, torsiyonel, bending) oluşumuna yol açar. Fiksasyonun rijiditesi, kırık uçların yüzey alanı, fragmanlar arası hareketi etkileyerek doku yüklenmesini ve kırık boşluğundaki hücre yanıtını belirler.…”