Acta chirurgiae orthopaedicae et traumatologiae Cechoslovaca

Acta chirurgiae orthopaedicae et traumatologiae Cechoslovaca

Souborný referát / Current concepts review

ACTA CHIRURGIAE ORTHOPAEDICAE ET TRAUMATOLOGIAE ČECHOSL.,
81, 2014, p. 355 - 364

Hojení zlomenin: kostní hojení jako výsledek fascinující kaskády fyzikálních a  biologických interakcí. Pokus o integraci pozorování z 30letého výzkumu AO v  Davosu. Část I.

Fracture Healing: Fracture Healing Understood as the Result of a Fascinating Cascade of Physical and Biological Interactions. Part I. An Attempt to Integrate Observations from 30 Years AO Research,

S. M. PERREN
AO Research Institute Davos, Switzerland

SUMMARY

The choice of best procedure in fracture treatment relies on a proper understanding of tissue reactions to the prevailing mechanical and biological conditions. Investing time and effort is rewarding as it opens up access to a  fascinating world and improves fracture treatment based on logical decision making.

An intact bony skeleton enables mechanical functions of the human body such as locomotion. This function of the bone is made possible by its stiffness and strength, which allows bone to carry load without undergoing major deformation while remaining intact even under heavy loads. The shortcoming of bone as a  strong and stiff material is its brittleness. Its brittle-ness prevents bone from bridging a fracture under unstable conditions. In spontaneous healing or healing under flexible fixation, a cascade of repair tissues stabilizes the fracture and allows for solid bony union.

Excessive load fractures the bone. Disrupted bone loses its stiffness. Loss of stiffness and, consequently, loss of skeletal support disables the function of the limb. Fracture healing is a ubiquitous and spontaneous process which restores stiffness as a prerequisite for mechanical function. Restoration of mechanical integrity requires that bone bridges and/or remodels the fracture site. If there is high initial tissue deformation (strain) at the fracture site, bone as a brittle material cannot bridge the gap. In spontaneous healing or healing under flexible fixation a cascade of consecutive phases of tissue differentiation are required to overcome this shortcoming of bone. The cascade increases tissue stiffness at the expense of tolerance to deformation until a  low value of interfragmental strain is reached that then allows bone to form a  solid bridge.

The cascade of differentiation is impressive as a "reasonable" process with a  goal. Therefore, bone healing is often considered as a rational process where the repair tissues are expected "to think and to act in order to achieve". We propose the observation of bone reactions without assuming that these reactions are guided by goal-oriented intelligence because the latter is non-existent. Observing the unexpected without having a preconceived opinion is a precondition for new insight. This approach avoids being misled into projecting one's own thinking into tissues that react without goal orientation.

Fracture healing is a repair process which requires induction and must be enabled. To get a feel for the problem we will first address the mechanical properties of bone as the prerequisites for its mechanical functions. Then we will discuss which conditions induce and which enable the repair process. The following paper addresses a fascinating interplay between physical and biological processes that enable fractured bone to bridge solidly and remodel to regain its "pre-fracture" function and structure.

No one of the different treatment modalities or healing patterns is best on its own. For a given situation the goal is to recover the function of the bone, limb and patient early and permanently by choosing the optimal procedure and implant. Understanding bone reactions permits a rational choice and replaces subjective predilection and monomania. The stability of the fixation and the blood supply are priority considerations, which must often be weighed against each other.

PREAMBLE

ACHOT 6/2014

The choice of best procedure in fracture treatment relies on a proper understanding of tissue reactions to the prevailing mechanical and biological conditions. Investing time and effort is rewarding as it opens up access to a  fascinating world and improves fracture treatment based on logical decision making.

An intact bony skeleton enables mechanical functions of the human body such as locomotion. This function of the bone is made possible by its stiffness and strength, which allows bone to carry load without undergoing major deformation while remaining intact even under heavy loads. The shortcoming of bone as a  strong and stiff material is its brittleness. Its brittleness prevents bone from bridging a fracture under unstable conditions. In spontaneous healing or healing under flexible fixation, a cascade of repair tissues stabilizes the fracture and allows for solid bony union.

Excessive load fractures the bone. Disrupted bone loses its stiffness. Loss of stiffness and, consequently, loss of skeletal support disables the function of the limb. Fracture healing is a ubiquitous and spontaneous process which restores stiffness as a prerequisite for mechanical function. Restoration of mechanical integrity requires that bone bridges and/or remodels the fracture site. If there is high initial tissue deformation (strain) at the fracture site, bone as a brittle material cannot bridge the gap. In spontaneous healing or healing under flexible fixation a cascade of consecutive phases of tissue differentiation are required to overcome this shortcoming of bone. The cascade increases tissue stiffness at the expense of tolerance to deformation until a  low value of interfragmental strain is reached that then allows bone to form a  solid bridge.

The cascade of differentiation is impressive as a "reasonable" process with a  goal. Therefore, bone healing is often considered as a rational process where the repair tissues are expected "to think and to act in order to achieve". We propose the observation of bone reactions without assuming that these reactions are guided by goal-oriented intelligence because the latter is non-existent. Observing the unexpected without having a preconceived opinion is a precondition for new insight. This approach avoids being misled into projecting one's own thinking into tissues that react without goal orientation.

Fracture healing is a repair process which requires induction and must be enabled. To get a feel for the problem we will first address the mechanical properties of bone as the prerequisites for its mechanical functions. Then we will discuss which conditions induce and which enable the repair process. The following paper addresses a fascinating interplay between physical and biological processes that enable fractured bone to bridge solidly and remodel to regain its "pre-fracture" function and structure.

No one of the different treatment modalities or healing patterns is best on its own. For a given situation the goal is to recover the function of the bone, limb and patient early and permanently by choosing the optimal procedure and implant. Understanding bone reactions permits a rational choice and replaces subjective predilection and monomania. The stability of the fixation and the blood supply are priority considerations, which must often be weighed against each other.

ACHOT 6/2014

MECHANICAL ASPECTS

a) The mechanical functions and characteristics of bone
ACHOT 6/2014

The mechanical functions of the skeleton require a rigid supporting structure for the muscles and articulations. If the tibia was likely to bend or buckle when bearing weight the muscles bridging the fracture could not maintain a  given position of the fracture fragments in relation to each other: Stiffness of bone is a prerequisite for the function of the limb. Strength of bone allows for resistance to load without failure. Apart from stiffness and strength a third mechanical characteristic is essential. It is the amount of deformation that a material undergoes before rupturing under increasing load. This is usually called "elongation at rupture" expressed as a relative unit such as percent (Fig. 1). A material with small elongation at rupture behaves like glass while rubber exhibits a large deformation at rupture. In turn glass breaks when a small deformation is imposed while rubber breaks after large deformation, bone is brittle like glass and connective tissue is tough like rubber. The element of bone (cortical and cancellous) breaks at an elongation of only 2% (17). As we will see the brittleness of bone is an essential characteristic that limits the contribution of bone to spontaneous healing and healing under non operative or flexible surgical fixation.

Here the issue is to understand how fracture healing is enabled through a  cascade of differentiating repair tissue and induction as well as bone resorption at the opposing surfaces of the fracture fragments (Figs 2 and 3).


ACHOT 6/2014
b) Mechanical characteristics of the fracture site during and after fracture

As high speed video recordings have demonstrated an explosive opening of the fracture site produces a void into which the soft tissues implode (Fig. 4). This is a process which results in a tissue-traumatizing implosion similar to cavitation. After the fracture has occurred the stiffness of the bone is disrupted locally and even small loading results in large displacement of the fracture fragments in relation to each other. After fracture and before treatment any repair tissue within the fracture gap is likely to undergo large deformation. Such large deformation is tolerated only by tissues that are tough. Prevailing conditions and characteristics of the tissue may be incompatible. Let's consider which procedures are required to enable final strong and stiff bridging of the fracture.


ACHOT 6/2014
c)Two different pathways that allow bony bridging

As mentioned bridging by any tissue can only occur when the tissue deformation in the fracture gap is below a given level, which depends on the elongation at rupture of the material and structure of the bridging tissue. Tissue deformation (strain) depends on the amount of displacement (mobility of the fracture) and, even more importantly, inversely on the width of the fracture gap (9).

Reducing fracture mobility

Immediately after fracture the following elements contribute to some reduction of the mobility of the fracture site:

- To minimize pain the body avoids loading of the fracture site.

- Pain-induced active tensioning of the muscles bridging the fracture. The tensioned muscles act as a sort of soft splint.

- The fracture hematoma and edema passively pre-ten-sion the tissues bridging the fracture gap.

- The hematoma displaces the soft tissue cuff and thus increases leverage of all tissues bridging the fracture.

- Under conditions of minimized loading even soft splints have an appreciable effect.

In the weeks after fracture the following tissue modifications essentially reduce fracture mobility:

- The soft cuff bridging the fracture undergoes differentiation to stiffer and stronger dense fibrous and/or fibro-cartilaginous tissue. The tissue stiffness from granulation tissue to cartilage increases by a factor to the power of ten.

- The diameter of the cuff increases and often reaches twice or more the diameter of the original bone. The resulting increase in stiffness may exceed physiological stiffness by ten times due to better leverage.


ACHOT 6/2014 ACHOT 6/2014
Reducing tissue deformation within the fracture gap
ACHOT 6/2014

The effect of the width of the gap on tissue deformation within the gap is as a rule not taken into account when the effect of stability or instability of the fracture is considered (10, 11, 12, 13). Let's look at reducing the mobility of the fracture and concomitantly at reducing tissue deformation further due to an increase in the width of the fracture gap due to surface resorption (Fig. 5).

As outlined earlier tissue deformation within the fracture gap for a given amount of fracture mobility depends on the distance of the moving fracture surfaces whereby the mobility has a proportional effect and the width of the gap has an inverse effect. Large strain may result in minimal fracture mobility if the gap is very small. As an example, a displacement of the fracture fragments of barely visible 0.1 mm results in 100% strain when the gap is only 0.1 mm wide. One would not expect such high amounts of strain in a  fracture situation where both displacement and gap width are barely visible.

Especially for a small fracture gap tissue deformation can be lowered by increasing gap width. The opposing fracture surfaces show a ragged structure of surface resorption that results in achieving a more or less equal distance between the surfaces. It has been shown that high strain at bone interfaces induces bone surface resorption that lowers strain (4).

Increasing the length of the bridging connection between two surfaces moving in relation to each other

A tissue bridge which spans a gap straight across, i.e. at the shortest distance from point to point between two moving surfaces undergoes the highest tissue deformation. If the bridge is structured in a three-dimensional way like a spring, the element of the spring undergoes small deformation in spite of the large overall displacement of the spring (Fig. 8). This is exactly what happens with the structure of callus which is appropriately called "woven" bone (Fig. 9). Callus acts like a spring. Once a small bridge is installed the increase in thickness and number of spanning elements immobilizes the bridge ultimately providing a solid connection.

Nonlinear stiffness as a function of tension in the initial repair tissues
ACHOT 6/2014

Of special interest is the fact that with increasing elongation the stiffness of connective tissue, for example, increases in a nonlinear way (17) (Fig. 10). Straightening of the ringlets of collagenous tissue seems to be the underlying mechanism. The effect of the nonlinear behavior of the material's stiffness is that a soft tissue that can tolerate the initial large deformation (strain) is able to limit the amount of movement. In this way a  gradual transition through the consecutive steps of differentiation is stimulated and enabled.

"Complete" elimination of fracture mobility by maintaining the fracture surfaces in close contact: compression fixation
ACHOT 6/2014

The mobility of a fracture can be eliminated by compressing the adapted opposing surfaces of the fracture. Compression keeps fragments immobilized through preload and/or by producing friction. When a fracture is exposed to a  bending load the surfaces of the fracture are compressed while surfaces on the opposed side of the fracture are unloaded and distracted. When the fracture surfaces are pushed together by application of compressive preload the surfaces remain in close contact for as long as the compressive preload exceeds the functional traction (Figs 11-13).

A classic example of transforming dynamic traction into compressive preload is the application of one or more wire loops, for example, in the application of a plate as a tension band on the traction side (Figs 14 and 15). When such implants are applied under some pretension traction produces bending. The distraction side of bending is protected by the wire while on the compression side the preload increases with traction.

The above statements consider the situation within the compressed surfaces. At the outer edge of such compressed surfaces one can expect that within a narrow zone from the outer bone surface inwards there is dynamic micro displacement with induced bone resorption and refilling (13) (Fig. 16 "gocce di cere", tear drop phenomenon).

Two side issues are worth mentioning here:

Precise reduction has often been advocated as a precondition for compression osteosynthesis. Precise reduction of the fracture is not a precondition for stabilization as such but facilitates tolerance of higher compressive load by distributing it over a larger contact surface thus reducing the critical load per unit area (stress). However, when ragged surfaces without precise reduction are compressed the contact peaks are squeezed until what is now a  larger contact surface reduces the stress (force/ area) below the strength (expressed as units of stress) of the bone.

As we will discuss later, rigid stabilization of a fracture using compression eliminates the fracture mobility that is a precondition for induction of fracture healing on the basis of callus. Under complete immobilization fracture healing by triggering callus formation is absent and fracture union depends entirely on internal remodeling. Such internal remodeling is similar or identical to the process we observe as the internal creeping 1 substitution of necrotic bone as in contact necrosis. With this in mind we understand "primary" healing as a side effect of internal creeping substitution (osteonal remodeling) induced by and replacing necrotic bone. This statement relies on the observation of remodeling of dead bone.

MECHANICS AND BIOLOGY OF DIFFERENT TREATMENTS AND HEALING

The following examples (Figure 17-Figure 25) demonstrate the different treatment modalities and their advantages and disadvantages based on different conditions of blood supply and mechanics of fixation.

Part 2 of the article will follow in the issue 1/2015.

References2

1 We use the term "internal creeping substitution" for a process of internal remodeling of the osteonal structure that keeps the overall stiffness and strength of the bone intact.

2 These references mainly concern the activity at the AO Research Institute. For an extensive List of Literature see Perren 2002

Celá stať v dokumentu PDF

Zpět


Nabídka nakladatelství:

 

Peter Wendsche, Radek Veselý et al.
Traumatologie

Traumatologie

Druhé, přepracované a rozšířené vydání

 

Jan Lebl, Zdeněk Šumník, Ondřej Souček, Hana Malcová, Klára Maratová, Jana Plešková, Štěpánka Průhová, Jan Štulík, Lukáš Wagenknecht
Onemocnění skeletu u dětí

Onemocnění skeletu u dětí

Motolské pediatrické semináře 4

 

Jiří Skála-Rosenbaum, Valér Džupa, Martin Krbec et al.
Zlomeniny proximálního femuru

Zlomeniny proximálního femuru

 

Jiří Kříž et al.
Poranění míchy

Poranění míchy

Příčiny, důsledky, organizace péče