After A Fracture, What Is The Correct Sequence Of Repair For Indirect Bone Healing?

"The virtually common complication of hand fractures is not malunion or infection. Rather, information technology is joint contractures and tendon adhesions."

Baratz and Divelbiss, 1997

Disquisitional POINTS

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Fracture reduction
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Fracture stability
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Soft tissue mobility
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Zone of injury (ZOI)
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Minimally invasive surgery (MIS)
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Clinical physiological correlation of tissue healing
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Clinical progression based on fracture healing and soft tissue response

Hand fractures do not occur in isolation. Every hand fracture has a proportionate closed or open injury to and response within its adjacent embedding soft tissues, creating a "zone of injury" (ZOI) ^,( Fig. 29-1A ). Immediately after fracture, a fundamental hematoma occurs inside the space between the fragments and expands about the fracture. Interstitial edema accumulates inside the impacted soft tissues and deposits fibrin as role of the astute inflammatory response to injury. The peripheral margins of the edematous response ascertain the ZOI ( Fig. 29-1B–D ).

Initial local signs of paw fractures include primary os deformity, secondary articulation deformities, movement and instability at the fracture site, pain, tenderness, swelling, ecchymosis, and heat. Without treatment, all of the tissues encompassed within the ZOI tend to become progressively spring into a single amalgam (1 wound/one scar) by the fibrin, fibronectin, and mucopolysaccharides ("tissue glue") contained in the extracellular matrix (ECM) ^,( Fig. 29-2 ). Joints adjacent to the fracture are ofttimes afflicted and can develop permanent intrinsic or extrinsic (or both) adhesions, stiffness, and deformity. Pseudoclaw deformities may develop ( Fig. 29-3 ). Tendons tend to adhere to side by side structures, sometimes impairing gliding. Progressive stiffness, cloudburst, dysfunction, and pain may issue ("fracture disease").

The essence of paw fracture direction is restoration of anatomic osseous integrity and stability throughout fracture healing; together with simultaneous preservation of the normal length and elasticity of the ligaments and joint capsules; and facilitation of early independent joint motion, tendon gliding, and functional recovery of the hand and digits. Gentle, progressive, controlled, passive range-of-movement (PROM) and unresisted active range-of-motility (AROM) exercises should exist initiated as shortly equally the fracture is reduced and stable. Early motion stimulates parallel interstitial collagen fiber alignment, which enhances scar elasticity and prevents or disrupts early adhesions in the interstitial spaces between disparate tissues during concurrent fracture healing and joint and tendon rehabilitation. The more than astringent the injury, the more than extensive and proliferative the fibroblastic response; and thus, the more compelling early on motility becomes. The duration and intensity of exercises are gradually advanced in accordance with the stability of the fracture, the response of the soft tissues, and the patient's hurting tolerance. The resting hand and digits should be positioned and protected in the functional (intrinsic plus) "prophylactic" posture between exercise sessions to prevent joint contractures and central slip attenuation.

Fracture and soft tissue healing are processes, non events that occur over time. Bone healing and scar formation undergo three discrete yet artificial and overlapping stages of progression: the astute or inflammatory phase, the reparative or proliferative stage, and the remodeling or maturation phase. Knowledge of the molecular and cellular interactions throughout the stages of bone healing and scar germination, the timing of events, and how these processes simultaneously interrelate within and adjacent to the mutual environment of the ZOI allows the physician and therapist to correlate incremental clinical functional rehabilitation with cellular and molecular events and tissue recovery. The medico, therapist, and patient must work together as a committed team to achieve the best result possible.

Fracture Illness

Immobility leads to so-called fracture disease. Fracture disease begins with uncorrected deformities of os and joints, astute hurting, and persistent edema. Without intervention, fracture disease evolves to include stiffness, tendon adhesion, capsular and ligamentous contracture or attenuation, central sideslip attenuation, infiltrative scar formation, and pseudoclawing. Additional edema may occur due to limb dependency, tight dressings, and pressure points over bone or articulation prominences. Consequently, fracture disease may spread across the ZOI and become complicated past local or regional chronic complex regional hurting (CCRP, reflex sympathetic dystrophy [RSD]). Articulation deformities may become progressively stock-still as early as three to 6 weeks afterward injury, and CCRP (RSD) may develop. Pain may become chronic, disproportionate to expectations, and unresponsive to ordinary treatment. Algodynia and hypersensitivity may occur. If undeterred, trophic changes gradually develop, including extensive fibrosis, brawny skin induration, shiny skin, digital tapering, loss of rugal blueprint, hair loss, smash growth changes, temperature and sweating abnormalities, and local or regional osteopenia. Fracture disease and CCRP become progressively recalcitrant to handling over time. Therefore, early intervention with fracture stabilization and digital exercises is essential.

Fracture Management

Ensuring anatomic fracture position and stability are the primary initial goals of hand fracture management. Hand fractures that are undisplaced and inherently stable practise not require reduction, merely do demand some protection against deforming forces and additional impact during early on healing. A small-scale cohort of manus fractures have inherent stability following manipulative reduction. They besides require the use of a protective static or functional orthosis for iii to 4 weeks. The remaining mitt fractures crave closed or open reduction and either temporary or permanent implant fixation to restore their anatomic integrity and stability as fracture healing and rehabilitation progress.

Early on fracture reduction and stability control pain, restore fracture surface apposition and the normal proportionate relationships between bone and next soft tissues, promote os healing, and provide a platform both for any necessary soft tissue repairs and for timely rehabilitation. Function follows form. Stability prevents "false movement" at the fracture site and allows revascularization and healing of repaired tissues to keep without disruption. Fracture fixation should exist every bit "atraumatic" equally possible to prevent or limit additional os devascularization, soft tissue impairment, and fibroplasia. Subperiosteal autopsy, flexor tendon sheath injury, and extensor tendon injury over the proximal finger phalanges in item, stimulate boosted fibroplasia.

Initial Treatment

Definitive fracture treatment may be delayed for upwardly to 5 to 7 days in closed, low-energy hand fractures having 2 fragments with petty alteration of event. Open fractures require urgent attention to débride, cleanse, and catalogue the wound; reduce the fracture; provide at least conditional fracture stabilization; and forestall infection. Simple (two-part) fractures with make clean, limited skin lacerations may exist safely and definitively stabilized and the peel repaired primarily. Soiled and complex wounds should initially exist left open and so ideally reassessed within 48 hours. Additional cleansing and debridement performed at that time should return almost wounds clean and suitable for definitive bone, tendon, and nerve and peel repair. ^,If not, the cleansing, debridement, and wound assessment may be repeated at 24- to 48-hour intervals until the wound is rendered make clean. The least invasive method of internal fixation should usually be selected from equally applicable methods.

Reduction

Although limb length, appearance, and part were probably somewhat impaired, primitive humans and animals in the wild have successfully healed markedly displaced, untreated fractures ( Fig. 29-4 , online). Early on indirect fracture healing evolved in an surround where mobility favored survival. The need to secure nourishment and avoid predators resulted in move about the fracture site that often stimulated callus formation. Over time it became evident that fractured basic held in anatomic reduction healed with ameliorate outcomes. The oldest tape of fracture reduction is constitute in Egyptian hieroglyphics (2450 bce ) depicting orthoses made from papyrus that were used to reduce and support distal forearm fractures ( Fig. 29-5 , online).

Shortening, angulation, and rotation are the chief elements of deformity and may be seen individually or in combination. Alterations of os anatomy may touch on functional consequence commensurate with their severity. Reduction restores the fracture fragments to their prefracture anatomy. Although a perfect reduction is of form ideal, the hand and digits have a remarkable chapters for functional adaptation to and tolerance of small and, sometimes, greater fracture deformity.

Anatomic Parameters and Functional Correlations

Recent reports have illuminated the correlation between deformity and functional loss and may help the physician to decide whether to have or correct a residue deformity. Manus dominance, occupation, or special individual needs may play a office. Observation of and discussion with the patient and the timing of presentation may also be critical in the decision-making process. The risk of postoperative digital stiffness may outweigh the benefit of bottom gains in anatomic fracture restoration in instances of pocket-size deformities, particularly in late-presenting inveterate fractures that take the early formation of a soft or hard callus that prevents closed manipulative fracture reduction.

Metacarpal Fractures

Metacarpal (MC) shaft fractures tend to angulate dorsally, owing to the unbalanced pull of the interosseous muscles and extrinsic finger flexors on the distal fragment ( Fig. 29-half dozen ). Intrinsic muscle shortening and altered muscle tension dynamics lead to increasing grip weakness after xxx degrees of dorsal MC angulation. There may also be loss of knuckle contour, pseudoclaw deformity, and a palpable or even visible MC angular deformity on the back of the hand, and prominence of the MC caput in the palm of the hand. The ring and pocket-size finger MCs are more tolerant of dorsal angulation than those of the index and middle fingers due to their increased carpometacarpal flexibility. Satisfactory results have been reported with as much as 70 degrees of dorsal angulation of subcapital MC (boxer's) fractures. ^,

Approximately vii degrees of extensor lag may develop for each 2 mm of residual finger MC shortening later fracture healing. The intermetacarpal ligaments ordinarily prevent greater than 3 to 4 mm of shortening of finger MC fractures. Internal MCs (third and quaternary) have more than restraint than edge MCs (second and 5th) since the distal fragment is anchored by intermetacarpal ligaments on both sides of the MC head. The intrinsic hand muscles contribute twoscore% to 90% of grip strength. ^,Every bit great as 8% loss of grip power may result from every ii mm of MC shortening. Based on this information, finger MCs may tolerate as much as three to 4 mm of shortening, and occasionally more, with only minimally noticeable clinical deformity and functional loss. In private instances, surgeons may cull to accept 3 to 4 mm or mayhap more shortening as an alternative to the risks of scarring and stiffness from surgical intervention.

Lateral MC angulation of 5 to 10 degrees may be tolerated, provided that no significant finger impingement occurs during move. MC angulation may exist best observed with the fingers straight, whereas impingement becomes more apparent as the fingers progressively flex.

The intermetacarpal ligaments between the MC heads provide some rotational stability to the distal fracture fragment. The internal MCs have more than restraint than edge MCs. Rotational deformity greater than 5 degrees may result in finger impingement, or "scissoring" (overlap). ^,Seitz and Froimson reported that 10 degrees of MC malrotation resulted in two cm of overlap at the fingertips. Rotational deformity of the fingers may exist apparent with total digital extension, but becomes progressively more pronounced equally the collateral ligaments tighten with finger flexion.

Phalangeal Fractures

Displaced fractures of the proximal phalangeal shaft characteristically display an apex palmar angulation (come across Fig. 29-half dozen ). The intrinsic muscles flex the proximal fragment, whereas the attachment of the key sideslip to the dorsal proximal border of the middle phalanx extends the distal fragment. The centrality of rotation of proximal phalangeal fractures lies on the fibro-osseous edge of the flexor tendon sheath. The distance of the moment arm from the rotational axis of the fracture site to the extensor tendons is greater than that between the axis and the flexor tendons, farther contributing to apex palmar angulation. Coonrad and Pohlman reported limitation of finger flexion with palmar angulation of greater than 25 degrees in extra-articular phalangeal fractures at the base of the fingers and advocated correction of greater deformities. More than recently, Agee reported shortening of the dorsal gliding surface of the proximal phalanx relative to the length of the extensor machinery if volar proximal phalangeal angulation exceeds 8 to fifteen degrees. As palmar angulation incrementally shortens the fractured proximal phalanx, the extensor mechanism may take equally much as 2 to 6 mm of reserve, owing to its viscoelastic adaptive properties, before the sagittal bands tighten to produce a progressive extensor lag at the proximal interphalangeal (PIP) joint of an average of 12 degrees for every millimeter of os–tendon discrepancy. Skeletal alignment sufficient to forbid or minimize extensor incompetence at the PIP joint and to restore the floor of the flexor tendon sheath is critical in the effort to restore both extensor and flexor tendon gliding and role. A persistent palmar athwart deformity of the proximal phalanx may lead to permanent attenuation of the fundamental slip, extensor lag, and pseudoclawing of the finger that may persist despite later correction of the osseous deformity. Apex palmar deformity of center phalangeal fractures manifests similar problems with skeletal shortening, extensor lag of the distal interphalangeal joint, and alteration of flexor tendon gliding and dynamics.

Stability

Although functional recovery (motion) is the ultimate overall goal of hand fracture management, stability is the ultimate purpose of reducing fracture fragments. Fractures that do non displace spontaneously or with unresisted exercises are considered stable. Inherently stable fractures safely tolerate incremental tendon gliding and articulation motion, maximizing their functional recovery. Reduced fractures that displace spontaneously or with unresisted movement cannot maintain their alignment. These fractures crave some grade of additional support or fixation to ensure that correct beefcake is maintained during fracture union. Fracture fixation methods vary from external to internal back up. Miniscrews, miniplates, tension band wiring systems, and "90-xc" wiring provide secure fixation and let healing to occur past direct bone formation. Less secure, "flexible" fixation methods, such as Kirschner wires (K-wires) and external minifixators, internally fix fractures. "Flexible" fixation allows nondisruptive micromotion at the fracture site, thus supporting and stimulating indirect bone healing. Flexible fixation permits sufficient exercising to preclude tendon adhesions and joint contracture in well-nigh instances. Exercises must initially exist restricted in their arc and intensity to prevent loss of reduction, wire migration, or pare and soft tissue irritation. Balancing the need to maintain fracture stability with the safe introduction of motion is based on scientific predictability and yet is the art and arts and crafts of mitt fracture direction.

Fracture configuration, impaction, periosteal disruption, muscle forces, and external forces may influence stability. Transverse and short oblique fractures have a stable conformation, whereas long oblique and comminuted fractures and those with bone loss have unstable patterns. Periosteal disruption correlates with the severity of the injury and the amount of fracture displacement. An intact or restored periosteum or bone impaction tin support fracture alignment. Unbalanced muscle or external forces can cause fracture displacement or collapse. The "safe" mitt position neutralizes the effects of muscle forces at the fracture site and thus, enhances fracture stability.

Fracture Stabilization

Nonoperative Management

Stable Undisplaced or Minimally Displaced Fractures

A majority of closed actress-articular hand fractures are simple (ii-fragment), undisplaced or minimally displaced, and stable, and therefore may exist safely and effectively treated past minimal protective orthoses and early on motion. This is especially true of impacted transverse or short oblique fractures at the base of the proximal phalanx and subcapital MC fractures with no rotational malalignment. ^,Indirect (secondary, enchondral, "biological," "physiologic," or undisturbed) os healing occurs.

Displaced Fractures That Are Stable Subsequently Closed Reduction

Airtight displaced transverse or short oblique unproblematic extra-articular manus fractures may oft be successfully reduced by closed manipulation (closed reduction, CR) and heal indirectly, or biologically. Fractures with elementary angulation are typically more than hands reduced. The cortices on the angulated side of the fracture human activity equally a hinge to implement reduction. The periosteum may be sufficiently intact to contribute to stability following reduction. Distal proximal phalanx fractures may take tenuous stability owing to their macerated cross-sectional area and the leverage of muscle forces at the fracture site. Successfully reduced fractures may require static immobilization for 3 weeks. External orthoses that protect the fracture and allow early ROM are optimal ( Fig. 29-7 ).

Internal Fixation

Indications

The physician must weigh the risks to benefits of nonoperative versus operative correction and stabilization for each fracture and deformity. Internal fixation is reserved for unstable fractures, irreducible fractures, lost closed reductions, comminuted fractures, fractures with bone loss, multiple hand fractures, hand fractures accompanied by ipsilateral extremity injuries, open fractures, and pathologic fractures. Secure stabilization may be advantageous for polytraumatized patients with a lower extremity long os fracture to facilitate patient treatment, transfers, and the use of crutches or a walker for ambulation. Hall has reported the advantages of using secure fixation in noncompliant patients. Maintenance of anatomic fracture position, wound admission, early edema management, and the ability to initiate early and intensive exercises are relative benefits of secure internal fixation.

When surgery is necessary, the medico must also cull amid approaches and implants. Fracture implants do not necessarily have to exist the strongest bachelor, but rather should be adequate in force to reliably hold the fracture through the early stages of fracture callus formation and maturation.

Minimally Invasive Surgery

Hand surgeons take long known the perils of indiscriminate open up reduction and internal fixation and have been among the kickoff to encourage minimally invasive surgery (MIS). MIS with closed reduction and internal fixation (CRIF) preserves periosteal integrity and circulation at the fracture site, minimizes expansion of the ZOI, allows for biological (undisturbed) fracture healing, and reduces the risk of additional adherent scar formation. ^,CRIF is advocated for unstable elementary closed manus fractures whenever possible. CRIF aligns the fracture fragments; avoids periosteal dissection, bone exposure, and disturbance of the blood supply; minimizes implant-to-bone contact; allows physiologic interfragmentary stress and strain; stimulates callus formation; and allows graduated exercise.

Transverse or short oblique phalangeal and MC fractures may be stabilized with unmarried or multiple intramedullary wires. Locking pins or subcortical buttressing of the wires at one or both ends of the fragments adds stability at the fracture site. Oblique closed diaphyseal phalangeal fractures may be stabilized with percutaneous transfixation wires. ^,Percutaneous wires may exist inserted transversely through an intact adjacent MC into one or both fragments of a closed elementary unstable MC fracture to provide fixation. Complex pilon fractures at the PIP joint can exist reduced and the articulation construction remodeled with the MIS percutaneous application of a transverse wire through the middle phalanx. The wire is dynamically attached to a moving component on an orthosis. Traction reduces the fracture length, while the intact and stretched periosteal sleeve compresses the fracture fragments ( Fig. 29-8 ).

Open up Reduction and Internal Fixation

Stable, or rigid, fixation is achieved at the price of a second planned wound to address the initial fracture injury. Sharp, depression-energy, neutrally placed incisions are less traumatic than random, high-free energy, edgeless bear upon, merely they nevertheless create additional fibroplasia. The greater potential for soft tissue scarring with open reduction methods may be partially offset by the opportunity for earlier and more intensive exercise.

Most paw fractures are approached with a dorsal incision. Surgeons should try to avoid violation of the peritenon between the skin and tendon and betwixt the tendon and bone as much equally possible. Incising the skin and MC periosteum to one side of the extensor tendon and placing retractors between the periosteum and the bone helps to accomplish this goal. Neutrally placed midlateral incisions and lateral ring retraction or excision may facilitate phalangeal exposure for selected proximal phalangeal fractures, minimizing the risks of tendon attrition, scarring, and intrinsic tightness that may occur with lateral ring incision and repair over an implant. Open fractures may oft be approached by extending the laceration or wound. It may exist prudent to secure the fracture with the almost stable bachelor implants that resource and the fracture configuration and operative exposure will allow.

Two or more miniscrews may exist used to secure and often compress an oblique diaphyseal fracture. Miniscrews may be thought of every bit small-scale direct K-wires with a head and threads. The screw head buttresses the next cortex while the threads grip the opposite cortex and heighten stability past compressing the fracture. The miniscrews protect each other from shear, rotational, and angle forces during rehabilitation and take the additional reward of remaining in place for the duration of fracture healing. Miniscrew fixation supports principal bone healing. Miniscrews are ordinarily removed simply if they become symptomatic.

Although the dissection required for plate awarding, particularly in closed fractures, is technically demanding and may devascularize adjacent os, delay bone healing, and generate additional fibroplasia, miniplates that compress the fracture provide excellent stability at the fracture site throughout healing. In open fractures, especially those with complex wounds, comminution, or os loss, priority must oftentimes be given to anatomic fracture restoration and healing. Secure miniplate fixation provides for earlier and more than intensive exercises than does flexible fixation and may at least partially showtime the disadvantages of operatively generated fibroplasia. "To operate on a fracture and fail to take advantage of the opportunity for early movement exposes the patient to the worst of both worlds: the injury is compounded and the potential gain is squandered."

Miniplates positioned dorsally under the extensor tendons or dorsal apparatus may restrict the extremes of digital move by their physical presence, especially as their edges arroyo adjacent joints. This is especially true of miniplates practical on the proximal phalanx adjacent to the PIP joint.

Straight miniplates are customarily applied to mid-diaphyseal fractures. Mini condylar plates accept a fixed angle bract or locking peg that may help in fracture reduction and may be applied either dorsally or laterally for juxta-articular fractures. ^,Principal or delayed primary bone grafting may be performed at the fourth dimension of plate awarding in near patients. Puckett and colleagues reported that microplates that allow closure of the periosteum take improved results in phalangeal fracture plating compared with larger miniplates that prevent periosteal closure. Fracture stabilization, os grafting when necessary, wound closure or coverage, and the initiation of rehabilitation inside three to 5 days of injury may provide the best opportunity for optimal functional recovery of open up or operated hand fractures.

Pathophysiology

Regeneration is the restoration of damaged tissue with cells of the aforementioned kind. Although some species such as lizards (east.1000., salamanders) and starfish can regenerate unabridged lost limbs, humans have retained this potential in just select tissues, liver, and bone, and to limited degrees. Peripheral nerves may regenerate distal to the prison cell bodies, and superficial skin lacerations regenerate true epidermis. About soft tissue injuries heal instead through a process of repair , in which fibrous scar tissue forms to weld the damaged cells. Scar, then, is the biological "glue" that allows tissues to heal that accept lost their regeneration potential. Bone heals by either primary or secondary regeneration. If the fragments are likewise distant from each other or insufficiently stable, regeneration cannot occur. ^,Conversely, small degrees of nondisruptive cyclic pinch at the fracture site stimulates secondary os regeneration and, later, bone remodeling.

Bone regeneration and soft tissue repair depend on complex processes—mechanoreception and cell signaling—to recruit migration of progenitor cells to the wound and to modulate proliferation and differentiation of these multipotential mesenchymal cells into cells capable of forming bone or scar tissue. This newly formed tissue must mature, strengthen, and reform its configuration to duplicate or gauge the original architecture and tissue function.

Bone must eventually heal with new bone by either passing through a temporary fibrocartilagenous phase prior to ossification (indirect healing) or through directly osteonal regeneration across the fracture site (straight healing). Both types of fracture healing ultimately lead to the regeneration of potent mature lamellar bone.

Indirect Bone Healing

Indirect fracture healing has also been called secondary healing, healing past enchondral ossification, or biological (undisturbed) bone healing. Indirect os healing evokes an evolutionary design wherein the requisite cellular response is matched to the wound surroundings to ensure that the repair process leads to os formation. A fusiform external callus surrounds the periphery of the fracture site and cascades through the entire spectrum of connective tissue from hematoma to granulation tissue, fibrous tissue, hyaline cartilage, woven bone, and, ultimately, lamellar bone to weld the fracture fragments and ultimately allow cancellous and medullary healing. Five factors are necessary for indirect bone regeneration: (1) a fracture hematoma as a source of signaling molecules, (2) a vibrant, diversified cell population to ensure healing progression and diet, (iii) an adequate claret supply, (4) an evolving scaffold for cellular differentiation, and (5) a mechanical environment of relative stability that minimizes interfragmentary strain. ^,This programmed sequence of tissue differentiation allows the most robust cells—fibroblasts and chondroblasts—to endure through an surround of compromised circulation, oxygen depletion, and instability until the metabolic and mechanical atmospheric condition are conducive to successful osteoblastic os replacement. Finally, fragile woven os is stress-remodeled into potent lamellar os. Cyclic reciprocal micromotion (compression–distraction) facilitates this process.

Inflammatory (Acute) Phase (Fourth dimension of Injury to Day 5)

The bones of the hand have a rich periosteal, intramedullary, and metaphyseal blood supply. No prison cell lies more than 300 µm from a blood vessel. Histamine-mediated vasodilation occurs during the offset several minutes following fracture. Whole blood pours into and expands the space nearly the fracture fragments and torn soft tissues, creating a liquid hematoma ( Fig. 29-9A , online). Local compression, secondary vasoconstriction, platelets, and the clotting cascade lead to the formation of a gelatinous blood clot. At that place are no functioning blood vessels in the fracture clot.

The hematoma and injured periosteum have important and complementary roles in the cellular events necessary for normal fracture healing. Consequently, early evacuation of the hematoma or excision or stripping of the damaged periosteum retards indirect healing. The claret clot contains growth factors, cytokines, and other complex peptides that stimulate neoangiogenesis and concenter white blood cells, macrophages, and multipotential mesenchymal cells to the fracture expanse. Within 24 hours after fracture, endothelial cells that line intramedullary capillaries overstate and migrate into the damaged area, initiating neoangiogenesis. Cells, nutrients, and cell-signaling peptides lengthened into the periphery of the claret clot from local soft tissues and new capillaries. White blood cells secrete lysozymes that dissolve the claret clot. Macrophages and osteoclasts phagocytize the clot and necrotic debris. Macrophages and platelets generate many of the boosted complex cell-signaling peptides that modulate mesenchymal jail cell differentiation and tissue development. Mesenchymal cells recruited from the damaged periosteum, next muscle, and regenerating blood supply differentiate into fibroblasts in the initially acidic and hypoxic environs and invade the periphery of the blood clot. The periosteum is the principal source of multipotent mesenchymal cells. Granulation tissue (fibroblasts and white claret cells) class the early pliable fusiform external fracture callus on the periphery of the claret jell and between the fragments.

Reparative (Proliferative) Stage (Day five to Day 21)

Healing past natural means (indirect or secondary repair) involves a gradual substitution of tissues that protects the fracture while bone is regenerated. Tissue oxygenation gradually improves and acidity proportionally decreases every bit neoangiogenesis progresses, facilitating centripetal healing of the external fusiform fibrous fracture callus from its periphery toward the center of the fracture. Mesenchymal cells now differentiate into chondrocytes rather than fibroblasts, until the gristly callus is replaced by nonmineralized hyaline cartilaginous scaffolding that encompasses the fracture site ( Fig. 29-9B , online). If the bone gap is not bridged by cartilaginous callus within two to 3 weeks subsequently injury, the initial callus response may neglect.

As stability increases, tissue oxygenation continues to improve and the ECM becomes alkaline. At 10 to 21 days after injury, the cartilage matrix begins to undergo progressive centripetal enchondral ECM calcification. Os morphogenic protein 7 (BMP-7), also known equally osteogenic protein 1 (OP-1), modulates new mesenchymal precursor cells to become osteoblasts. The new osteoblasts invade the cartilaginous callus to class immature trabecular "woven bone" across the fracture site. Cartilage cells undergo apoptosis and are removed by chondroclasts. From the 2d to the sixth calendar week after injury, intermittent axial compression can increase corticomedullary blood flow and stimulate chondrogenesis and, later, osteogenesis throughout the callus. Conversely, excessive shearing motion during this time tin impede neoangiogenesis and delay or prevent fracture healing past dissentious new arterioles and capillaries. Throughout this procedure, the external fracture callus progressively solidifies and becomes stronger. The periosteal, intracortical, cancellous, and intramedullary blood flow normalizes. Intramedullary healing proceeds. Interfragmentary motion (IFM) progressively decreases and finally ceases at approximately 4 to 6 weeks after injury. At this indicate the fracture is clinically stable, even though radiolucent portions of the fracture may be seen on radiograph.

Remodeling (Maturation) Stage (Mean solar day 21 to 18 Months)

The reparative phase of healing extends into the remodeling phase. The initially accreted immature woven bone is randomly aligned and weaker than normal lamellar bone. The ideal goal of fracture healing is to regain the original course and role of the healed bone ( Fig. 29-9C ). Progressive remodeling of primary immature trabecular bone forth the lines of axial stress forms meaty lamellar bone (Wolff's constabulary) and reestablishes the Haversian canals. During this process, osteoclasts remove the weaker woven bone from the tension sides of trabeculae, and osteoblasts accrete linear layers of mature new os on the pinch sides parallel to the stress forces. Osteoclastic metabolism (bone resorption) is initially 50 times greater than osteoblastic activity (bone accretion). This initial imbalance creates temporary local os porosity that facilitates neovascularization into the Haversian canals. Bone remodeling and metabolic equilibration takes approximately v months to complete in the tubular basic of the hand. These forces direct the orientation of newly formed bone to provide better mechanical advantage and duplicate the original shape and strength of normal bone. Each region of each bone responds to a particular corporeality of intermittent strain, creating an "optimal strain surroundings" for remodeling. ^,Static loading has picayune influence on bone compages. A distinctive "dose/response" curve is generated by daily brusk, intermittent stimulation exposure with strain magnitudes within the physiologic safe range for the bone. Fracture remodeling is optimally influenced by a regimen of dynamic, diverse activities that do non exceed the strain tolerance level of the bone. Remodeling does not e'er occur simultaneously in all areas of the fracture. The injured os regains approximately 80% of its original strength within 3 months after fracture, although 18 to 24 months is often required to regain normal tensile force.

Remodeling allows some correction of angular deformities along the lines of linear stress in younger children, and occasionally in adolescents and adults, simply does not right rotational deformities. The ability of bone remodeling to correct athwart deformities past remodeling diminishes with age.

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