Physis is the weakest structure in the skeleton of a child and a frequent site of an injury or fracture. A physeal fracture presents a unique challenge in the management as the sequalae of such an injury could lead to growth disturbances.
In this review, mainly focussing on traumatic physeal injuries, the authors discuss the applied anatomy, different fracture patterns, clinical assessment and management of physeal fractures in children.
Discussion on acute physeal injuries as well as physeal arrest and approach to its management is presented. Past attempts for treatment of physeal injuries and recent advances in their management is also discussed.
The ideal approach to treat physeal injuries should take into account the location of injury, age of the patient, fracture type and growth potential of the involved physis. Prompt diagnosis and physeal-respecting treatment techniques are important.
Keywords: Physis, Fractures, Growth, Arrest, Management, ReviewPhysis (growth plate or epiphyseal plate) is the cartilaginous disc present at ends of a long bone and is responsible for the longitudinal growth of the bone in a child. Physis is the weakest structure in the skeleton of a child and is thus, a frequent site of an injury or fracture. An injury which would cause a ligamentous sprain of a joint in an adult, would cause a physeal fracture in a child. Several factors must be considered while evaluating a child with a physeal fracture like the age of the patient, location of the physis, fracture type and growth potential of the involved physis [1]. A physeal fracture presents a unique challenge in the management of the child as the sequalae of such an injury could lead to growth disturbances. These growth disturbances could manifest as limb length inequality or angular deformities. Of all the physeal fractures, growth arrest or disturbances are seen in 5–10% of the cases [2].
In this review, we discuss the applied anatomy of the physis, different physeal fracture patterns, clinical assessment of a child with physeal injury and management of physeal fractures. We briefly discuss physeal arrest and approach to its management. Lastly, we would review the past attempts for treatment of physeal injuries and recent advances in their management. Although physeal injury can result from infection, malignancy, metabolic abnormalities or iatrogenic damage, the current review would be limited to traumatic physeal injuries or physeal fractures.
Physeal fractures account for 30% of all the paediatric fractures [3]. These fractures are more common in adolescence as in a younger child, the epiphysis is more cartilaginous and acts as a shock absorber with significant amount of forces been transmitted to the metaphysis [4]. Boys are affected twice as often as girls as their physis remain open till a later age and they may be more susceptible to trauma due to increased sports participation [3, 5–7]. Regardless of the site, distal physis are more commonly involved than the proximal physis with distal radial physis as the most frequent site to be involved followed by distal tibial physis [3, 5–7].
To effectively manage physeal fractures, it is essential to understand the anatomy of the physis (Fig. 1 ). Long bone development begins at 6th week of intrauterine life as condensation of the mesenchymal anlage. By 8 weeks, a primary ossification centre develops in the middle of long bones. The primary ossification centre grows by endochondral ossification and extends towards the end of the long bones. On radiographs, the physis is visible as a radiolucent zone separating the metaphysis and epiphysis at the end of long bones. It is also referred to as metaphyseal or primary physis. This is to distinguish it from articular [8] or secondary physis [9] which is responsible for growth of the secondary ossification centre of the epiphysis towards the joint. The word ‘physis’, by default, refers to the primary physis. Relative contribution of different physis to longitudinal growth and absolute amount of growth per year is given in Fig. 2 .
Structure of physis
(Source: Mallick A, Prem H. Physeal injuries in children. Surgery (Oxford). 2017 Jan;35(1):10–7.)
Relative contribution to growth by various physis
(Source:Lippincott Williams & Wilkins from Lovell and Winter’s Pediatric Orthopedics, Morrissy R.T. and Weinstein, S.L. (Eds), 2005)
The periphery of the physis is attached securely to the metaphysis through the Zone of Ranvier and Ring of LaCroix. The Zone of Ranvier is a groove around the periphery of the physis that contains chondrocyte progenitor cells and is responsible for the circumferential growth of the physis [10]. The Ring of LaCroix is a fibrous continuation of periosteum and provides mechanical support to the physis [4].
Physis is made up of hyaline cartilage and it consists of chondrocytes organized in columns along the long axis of the bone. It is divided into four zones from epiphysis to metaphysis: Germinal, Proliferative, Hypertrophic and Endochondral Ossification. The germinal layer includes chondrocytes in somewhat inactive state. The proliferative layer includes chondrocytes that undergo rapid mitotic division and are organized in stacked columns. These two layers are rich in extracellular matrix and collagen fibres and are therefore able to resist shearing forces [11]. In the hypertrophic zone, the chondrocytes lose their ability to proliferate and differentiate in to mature chondrocytes with increased cell volume. The extracellular matrix and amount of collagen fibres are negligible. Therefore, hypertrophic zone is weaker in comparison to other zones and most of the physeal fractures occurs through this layer. In the zone of provisional calcification, the chondrocytes undergo apoptosis and the cartilaginous matrix begins to calcify. These islands of calcified cartilage act as scaffold for new bone formation, facilitated by invasion of capillaries from the metaphysis. The osteoclasts and osteoblasts from the metaphysis break down the calcified cartilage and replace it with mineralized bone.
Physeal injuries heal faster than bony injuries. Typically, a physeal fracture would heal in 3–4 weeks. However, in case of an injury to a large undulating physis, like distal femur physeal fracture, the fracture plane would traverse through various zones of the physis. Likewise, intra-articular physeal fractures, like Salter–Harris (SH) type III and IV fractures, would traverse through various or all zones of the physis. Such injuries have worse prognosis as the chances of bone formation across the physis increases when multiple zones are injured.
Knowledge of the blood supply in and around the physis is necessary to understand the consequences of physeal fractures. Physis receives its predominant blood supply from the epiphysis (Fig. 3 a). Other sources of blood supply are from the metaphysis and the perichondrial ring [13]. Epiphyseal circulation essentially supplies the germinal and proliferative layers of the physis. It is further divided into two types by Dale and Harris (Fig. 3 b) [12]. In type A, the epiphysis is entirely covered by articular cartilage and receives its blood supply from vessels that enter the epiphysis by traversing the perichondrium at the periphery of the plate. Thus, physeal separation or injury, as in femoral neck physeal fracture, could lead to destruction of the blood supply to the epiphysis and resultant avascular necrosis. In type B, the epiphysis is partially covered by articular cartilage and receives its blood supply by vessels that directly penetrate the epiphyseal cortex at areas that are not covered by articular cartilage. Thus, physeal injury would lead to temporary interference with endochondral ossification marked by increased thickness of the physis, followed by rapid healing within 3–4 weeks.
a Blood supply to physis and b types of epiphyseal blood circulation to physis (Image
Source: Mallick A, Prem H. Physeal injuries in children. Surgery (Oxford). 2017 Jan;35(1):10–7.)
The metaphyseal circulation comes from the branches of nutrient artery and they supply the zone of endochondral ossification. The perichondrial ring of LaCroix supplies the periphery of the physis. It is evident from the above discussion that hypertrophic zone remains relatively avascular.
The most widely used classification system for physeal fractures is the Salter and Harris classification system, (Fig. 4 ) which divides the physeal injuries into five types. [14] This classification system helps guide the treatment as well as prognosticate the facture pattern. Types I and II are extra-articular fractures with good prognosis. These fractures mostly occur through the hypertrophic zone of the physis and have significantly lower rates of physeal arrest. Types III and IV are intra-articular fractures that would typically involve various or all layers of the physis with increased potential for physeal arrest. Type V fractures are diagnosed in retrospect after the occurrence of growth arrest and deformity. Rang added a type VI fracture that involved the periphery of the physis, including the perichondral ring (Fig. 4 ) [15]. This injury and loss of peripheral physis is typically seen around an open injury to the medial malleolus. Peterson described a classification system in which the initial four types of Salter–Harris classification were retained while adding two new types (Fig. 4 ) [9].
Classification of physeal fractures (Images
source: Mallick A, Prem H. Physeal injuries in children. Surgery (Oxford). 2017 Jan;35(1):10–7.)
The initial investigation usually done to diagnose physeal injuries are plain radiographs. The radiographs should include two orthogonal views and should focus on the site of fracture to appreciate the true injury pattern and displacement. It is not recommended to evaluate distal radius physeal fractures on forearm radiographs or ankle physeal injuries on full leg radiographs. The extent of injury would be unappreciated on such views due to parallax, image distortion, magnification errors and inadequate visualization. Other radiographs should incorporate a joint above and joint below the site of injury. When in doubt or when ossification variants mimic fractures, contralateral radiographs can help. Sometimes, an oblique view is required to better portray the fracture pattern, as in the internal rotation oblique view to evaluate fracture of lateral condyle of distal humerus. Stress views are not recommended as it can displace the fracture, can cause iatrogenic injury to the physis and can cause significant discomfort to the patient.
Although MRI can be used to diagnose occult physeal fractures, its value and usefulness in paediatric trauma is limited. Gulfer et al. detected occult physeal fractures around the elbow, ankle and knee in 8 of the 23 patients (34%) who presented with clinical symptoms and signs of injury, but had negative radiographs [16]. MRI is recommended for evaluation of traumatic haemarthrosis of a joint without an apparent fracture. For example, TRASH (The radiographic appearance seemed harmless) lesions of the elbow joint would be a primary indication for MRI [17]. MRI can also be helpful for assessment of chondral/osteochondral injuries and ligament injuries of major joints [18–21].
CT scan is recommended for delineation of fracture lines and for preoperative planning for intraarticular physeal fractures, mainly around the knee and the ankle [22]. In a study comparing CT scan and radiographs of triplane ankle fractures, the CT scan changed the diagnosis in 46%, changed the treatment plan in 27% and changed the number and trajectory of the screws in 41% patients, as compared to radiographs [23]. Thus, CT scan can help to delineate intra-articular fracture geometry and aid in treatment planning. Besides this, CT scan can be used for 3D assessment of complex injury patterns or their sequelae, i.e. growth arrest, deformity or malunion [24, 25].
Intraoperatively, an arthrogram can provide valuable information by outlining the largely cartilaginous articular surfaces and is routinely used in paediatric trauma [26]. It not only provides information about articular surface gap or step-off, but also aids in the placement of percutaneous fixation by delineating the chondral surface. An arthrogram can be performed for any joint to evaluate the articular surface, but is more commonly used around the elbow joint.
Partial or complete growth arrest is one of the most significant complication of a physeal fracture. Partial arrest is classified into: central, peripheral, linear or combined depending upon the location of physeal bar (Fig. 5 ). It is essential to assess the exact location and size of the physeal bar and estimate remaining growth, to help formulate management decisions [27]. Plain radiographs of the involved and contralateral uninvolved physis can provide general information about the physeal bar. Serial plain radiographs can be used to evaluate for any developing deformity or limb length discrepancy. A left-hand bone age radiograph can help to estimate remaining growth. For assessment of the physeal bar, a CT scan can help to determine the exact location and size of the bony bar and create physeal bridge map. The drawbacks of CT scan are that it does not provide information about a fibrous bar or about health of the remaining physis [28]. Moreover, there is a small risk of radiation to the children. MRI is the imaging modality of choice for assessment of physeal bar and specialized software or manual calculation can help to map the area of physeal arrest [29].
Classification of physeal bar (Images
source: Mallick A, Prem H. Physeal injuries in children. Surgery (Oxford). 2017 Jan;35(1):10–7.)
The following principles are recommended to manage physeal injuries in children with some modifications depending upon location of injury and age of the child.
Displaced physeal fracture should be reduced with sustained traction and gentle manipulation. Forceful reduction manoeuvres, repeated attempts of reduction or insertion of instrument in to the physis to manipulate fracture fragments should be avoided as it could grate the physis and cause iatrogenic physeal injury. Open reduction is better than multiple attempts at closed reduction.
For an extra-articular physeal fracture (SH 1 and 2) delayed reduction attempts beyond 5 days after injury should be avoided. Such attempts could lead to iatrogenic physeal injury and resultant growth arrest. Instead, it is better to allow the fracture to heal and remodel. Management of malunion is relatively easier than management of growth arrest in a young patient.
Intra-articular displaced physeal fractures (SH 3 and 4) should be reduced anatomically and stabilized by internal fixation, irrespective of their time of presentation. Articular surface congruity and reduction is of utmost importance. The reduction can be achieved by closed, arthroscopic or an open approach.
Implants used for internal fixation should be placed in a physeal-respecting manner. They should be placed parallel to the physis when the fracture geometry allows for it. If an implant is placed across the physis (transphsyeal), compression should be avoided. If more than 2 years of growth is remaining, the transphyseal implant should be removed once the fracture is healed.
There are several methods for assessment of accuracy of articular surface fracture reduction for SH 3 and 4 physeal fractures. These include direct visualization, fluoroscopy, arthrogram or arthroscopic assessment.
Resecting a small portion of periosteum on either side of the physis during an open reduction of fracture may help to reduce the risk of bony bar formation, although this is controversial [22].
For an exposed or crushed physeal injury, an acute or anticipatory Langenskiold procedure (use of free fat graft to cover the physis) can be performed to help prevent growth arrest [30, 31].
Most physeal fractures heal in 3–4 weeks.Growth arrest lines (Park–Harris lines) are transverse lines seen in the metaphysis (Fig. 6 ). Their orientation and relationship to the physis are used to assess growth and growth disturbances [32, 33].
Growth arrest lines normal and abnormal Park–Harris (PH) lines. a Arrows point to normal PH lines which are parallel to physis. b Dashed arrow points to area of physeal arrest. PH line is not parallel to the physis and coverages towards the area of growth arrest
For a displaced physeal fracture, the patient should be monitored for growth disturbances for at least a year or until the patient is skeletally mature. For undisplaced physeal fracture, there is no need for serial radiographs. Instead, the family should be counselled about low potential for growth arrest and to follow-up if any symptoms or deformity are noticed.
Iatrogenic injuries to physis can be caused by forceful reduction manoeuvres or due to placement of periphyseal or transphyseal implants (Fig. 7 ). At times, it is difficult to differentiate iatrogenic injuries from the initial injury insult. Physeal arrest (SH V) has been reported after metaphyseal and diaphyseal fractures not involving the physis [34]. Similarly, inadvertent physeal injuries can occur during routine treatment of metaphyseal and diaphyseal fractures. Several factors decide the fate of physis after an initial injury.
Forceful and repeated manipulation of physeal fracture could lead to increased physeal damage. For extra-articular physeal fractures, satisfactory alignment of the fracture fragments is acceptable rather than forceful attempts to achieve anatomic reduction. Physeal gap of up to 3 mm may be due to periosteal interposition in the fracture fragment. It is not necessary to remove this interposition as it has not shown to affect the rate of premature physeal closure [35]. If the fracture fragments cannot be aligned and there is persistent deformity after reduction attempts, then open reduction should be performed to remove any tissue interposition.
K-wires: several animal studies have shown a correlation between transphyseal pinning and growth disturbances [27, 36, 37]. Premature physeal arrest has been reported after pinning of distal radius fracture by several authors [38–40]. Boyden and Peterson observed that premature physeal closure was potentially related to pin size, location of the pin within the physis, obliquity of the pin within the physis, use of threaded pins, and increased duration of retention of pin in the physis [38]. Smith et al. showed that the use of temporary transphyseal pinning in juxtaphyseal fractures of upper limb, resulted in physeal arrest in 1 out of 5 patients on MRI evaluation at 6 months after the removal of K-wire [41]. Thus, transphyseal K-wires should be used judiciously across the physis and multiple K-wires, multiple attempts at insertion of K-wires, large-size K-wires, intrafocal K-wires and permanent K-wires should be avoided.
Intramedullary Nails: Piriformis entry of intramedullary rigid nail for treatment of femoral diaphyseal fractures in children can lead to avascular necrosis of the femoral head (due to vascular injury) or coxa valga (due to injury to the medial aspect of trochanteric apophysis). This has been observed in 30% of the cases in one series [42]. This did not depend upon the dimension and duration of retention of nail [43]. Another study showed that physeal arrest developed in three out of the eight patients following nailing due to reaming [44]. Trochanteric entry or lateral entry nail have shown to minimize such complications. Other authors showed favourable result with nailing when the nail was placed in the centre of the physis and diameter of the nail was small in relation to the physis [45]. Similarly, injury to distal femoral physis could happen during placement of retrograde flexible intramedullary nails. It is recommended that insertion point for such nails should be in the metaphysis and dissection should be avoided in the area of the physis during nail placement.
Threaded pins and screws: threaded pins and screws across the physis are avoided due to potential risk of premature physeal closure except in some instances. For example: threaded K-wires/Steinmann pins are used for fixation of displaced proximal humerus physeal fractures. Smooth K-wires have shown to migrate when used around the shoulder area as early as 5 days after placement, and may end up in vital structures (lungs, heart, vessels, mediastinum) and could be fatal [46]. When threaded implants are placed across the physis, it is recommended to remove these implants after fracture healing.
An example of iatrogenic physeal arrest following ORIF of tibial tubercle fracture-Physeal arrest could be due to primary injury but keeping screws across physis after fracture healing in a growing child would lead to iatrogenic growth disturbances. This could be potentially prevented by the removal of screws after fracture healing
Physeal arrest (bony bar, physeal bar, bony bridge) leading to growth disturbances occurs in about 5–10% of physeal fractures [2]. Growth disturbances are always a possibility after injuries around the physis and the family should be counselled about it at the start of the treatment and the information should be reinforced periodically during follow-up. The follow-up radiographs should be carefully scrutinized to detect early signs of growth disturbances. An anatomic reduction, with or without internal fixation, does not guarantee against a growth arrest. Management of physeal arrest would depend on the physis involved (location and extent), type of bony bar (location and size), growth remaining and existing or expected deformity/limb-length discrepancy [47, 48].
Minor disturbances in physis are seen in a high percentage of physeal injuries, but may not require any treatment except for observation. Several animal studies have concluded that injury to 7–10% of the physis did not result in permanent growth arrest and may not require any treatment [49–51]. On rare occasion, a small bony bar may break due to continuous longitudinal growth of the uninjured physis [52]. This would typically occur in younger patients when the physis has significant growth potential. Sometimes, the physeal bar may resolve spontaneously [53–56]. An atypical incomplete bar (forme fruste bar) due to cartilaginous aberration may be seen after physeal fracture. It is due to increased production of physeal cartilage which could temporarily tether the growth and cause growth disturbances. Possible explanation for this phenomenon is temporarily cessation of blood flow to the metaphysis delaying the invasion of the cartilage columns in the hypertrophic zone by the vascular and bone forming activities of the zone of provisional calcification [57].
The principles of management of physeal arrest are summarized in Fig. 8 . This is a simplified flowchart to help with complex decision-making process. Assessment of the remaining growth is based on the skeletal age and not chronological age. Although it has been reported that a physeal bar occupying up to 50% of physeal area could be successfully removed, 30% seems to be a threshold based on the recent reports and authors experience. Similarly, the general indications for hemiepiphysiodesis and osteotomy have been listed here as > 5° and > 10° of deformity, respectively. This may vary based on the physis, remaining growth and physician–patient–family shared decision. [58].
Flowchart showing principles of management of physeal arrest
Acute Langenskiold procedure Langenskiold popularized the method of free fat graft interposition after resection of partial physeal arrest. The fat graft would prevent reformation of the bony bridge. Similar concept could be used in an acute setting. With high-risk fractures, like SH IV and VI, when the physis is crushed or exposed, an acute Langenskiold procedure can help prevent a bony bar [31]. Foster et al. reported two cases of SH IV fracture and one case of SH VI fracture treated with acute free fat grafting over the exposed physis. Based on their excellent results and success in prevention of bone bridge formation, the authors recommended a definite role for an anticipatory Langenskiold procedure in the management of acute high-risk physeal injury [30]. Recently, Abbo et al. reported on an SH VI fracture of distal tibia in an 11-year-old boy, where an anticipatory Langenskiold procedure was performed successfully using bone cement instead of fat graft [59].
Interposition materials They are used after bony bar resection in order to prevent accumulation of blood in the cavity which can lead to recurrence of bar formation. Various interposition material used are fat, polymethylmethacrylate (PMMA), silastic, cartilage, bone wax and dura. Fat and PMMA are the two most commonly used interposition materials [9]. Fat has the advantage that it’s nonimmunogenic and can be harvested locally. The disadvantage is that it is not haemostatic and tends to float out of the cavity when the raw bone surfaces bleed after the removal of bony bar. Application of either thrombin or bone wax can provide haemostasis and help prevent fat migration. The other option is to suture the fat to the epiphysis and metaphysis using drill holes. Langenkiold recommended suturing ligament, muscle or subcutaneous tissue over the fat to prevent migration [60, 61]. Another disadvantage of fat is that it does not provide structural support to the weakened bone, thereby predisposing the bone to pathologic fracture. Thus, postoperative immobilization and limited weight bearing may be required [62]. Lastly, fat cells can undergo degradation or necrosis that can lead to recurrence of bony bar formation [63]. PMMA without barium (Cranioplast) has several desirable characteristics like being inexpensive, minimally thermogenic, easily available, inert, haemostatic and radiolucent. It can provide structural support after bone bridge resection and thus early weight bearing could be initiated [64]. When used as an interposition material, PMMA should be tethered to the epiphysis to prevent it from migrating into the metaphysis. This can be achieved by creating drill holes in the epiphysis, using K-wire through the epiphysis and PMMA or by undermining the epiphyseal walls to create PMMA plug anchor.
Fibrin (fibrin glue, fibrin sealant) is routinely used for its haemostatic and surgical sealing properties and is easily available in the market. Its role in prevention of bony bar has been explored in animal models. Besides minimizing bleeding at the site of physeal injury, it can create a microenvironment that is suitable for chondrocyte induction and conduction [65]. Jie et al. reported that fibrin could effectively inhibit bony bar formation in a proximal tibia physeal injury rat model. Fibrin application led to the formation of a scar-like tissue instead of a bone bridge [66]. In a porcine model of distal femur physeal injury, Abood et al. reported that fibrin alone could prevent formation of bone bridge in 4 of 5 specimens and was more effective than fat as interposition material. When fibrin was mixed with autologous articular cartilage, the mixture prevented bone bridge formation in all specimens [67]. Thus, fibrin appears to be an attractive, readily available, alternative to other interposition materials although its clinical results are lacking.
Physeal distraction Symmetric distraction of physis by an external fixator has been used for bone lengthening in children [68, 69]. In animal studies, the rate of distraction had an effect on the fate of the physis as rapid distraction (1 mm per day) led to ossification and closure of the physis but slow distraction (0.25 mm twice a day) maintained the normal physeal thickness and growth potential [70]. These principles have been applied to post-traumatic physeal bar and resultant growth deformities. Slow, asymmetric physeal distraction could potentially break the physeal bar and allow for deformity correction followed by normal physeal growth. Aldegheri et al. reported on 35 lower extremity post-traumatic deformities and their best results were achieved when the bone bridge occupied less than 20–30% of the physis [71]. Canadell and De Pablos reported on eight cases with bony bar and deformities affecting the lower extremities. They reported adequate correction with physeal distraction without the need for resection of the bone bridge [72]. Bollini et al. reported successful treatment of a centrally located bony bridge of the lower tibia using distraction by Ilizarov technique [73].
Physeal transplantation An alternative to the treatment of physeal bar would be to exchange it with normal functioning physis to produce meaningful growth. The physeal transplant could be an autograft or allograft and it could be vascularized or non-vascularized. Autograft availability of physis is significantly limited by lack of donor site in the body. Possible donor sites for physeal cartilage include proximal fibula, distal ulna, distal clavicle, phalanx, toe, costal cartilage or iliac crest apophysis. The physis could be transplanted as a bone block (containing sliver of epiphysis and metaphysis with intervening physis), as the end of a bone containing physis or as part or whole physeal plate without bone. Mayr et al. reported on 3-year follow-up of successful reconstruction of medial malleolus defect in a 10-year-old boy using iliac crest apophyseal cartilage and physeal transplant [76]. Gigante and Martinez reported on 4-year follow-up of a successful case of excision of bone bridge from distal radius physis in a 12-year-old boy and replaced it with an autologous block from iliac crest apophysis [77]. The cartilaginous transplant was oriented such that the bony part of the iliac crest was placed against the metaphysis of the radius. Despite clinical case reports and encouraging animal study results, physeal transplant is not popular as the results are unpredictable. The donor site is limited and the donor physis retains its growth potential which may be different from the growth rate of the recipient site [78, 79]. The physis has to fit exactly at the recipient site so that the metaphysis and epiphysis are aligned appropriately. Slight mismatch could lead to bony bar formation. For non-vascularized grafts, inadequate vascularity and nutrition could lead to ischaemia and death of the physis [80]. To obviate the issue of limited donor site availability, physis allograft transplantation has been studied in animal models. Microvascular transplantation of physeal allograft is appealing but its use restricted due to lack of data on the survival of cartilage cells in the physis and the risk of immunogenic reaction in the host, which would require immunosuppressive therapy [81].
Regenerative and tissue-engineering approaches Various studies have proposed newer approaches which suggests that, not only the bony bar formation be prevented but can also be regenerated to healthy physis. Autologous chondrocytes embedded in scaffolds have been successfully integrated into growth plate in animal models [82, 83]. However, their use may be limited by the need to isolate chondrocytes from normal tissues, thus creating secondary injury sites. To counter this, mesenchymal stem cells (MSCs) from periosteum and bone marrow have been used. These MSCs resulted in native like repair tissue in animals [84]. To promote cartilage differentiation of cells, chondrogenic factors such as IGF-1, TGF BETA-1 and 2 are commonly used [85]. For cells and chondrogenic molecules to have an effect at the site of physeal injury, they have to be delivered locally by a temporary scaffold. Commonly used scaffolds are collagen I and II, hyaluronate–collagen–fibrin composites, Collagen chitin scaffolds, agarose, chitin, gelatin and PLGA. Another potential approach is to modulate the pathways that stimulate osteogenesis. Bevacizumab, a humanized anti-VEGF antibody, showed reduction in osteogenic gene expression, fewer blood vessels, and decreased bony bar formation [86]. Other pathways which have been studied include Wnt/β catenin. Inhibition of this pathway in rat models have led to decreased bony bar formation [87]. Thus, the field of regenerative medicine holds a lot of promise for the future.
Physeal fractures are common. The ideal approach to treat these injuries depends on thorough understanding of principles of physeal fracture management, taking into account the location of injury, age of the patient, fracture type and growth potential of the involved physis. Prompt diagnosis and physeal-respecting treatment techniques are important but may not be sufficient to prevent future physeal growth arrest and resultant growth disturbances. Family counselling and careful vigilance would help in identification and management of such growth disturbances should they occur.
The authors declare that they have no confict of interest.
Ethical standard statementThis article does not contain any study with human participants performed directly by any authors for this particular paper.
Informed consentFor this type of study informed consent is not required.
Publisher's Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
1. Dodwell ER, Kelley SP. Physeal fractures: basic science, assessment and acute management. Orthopaedics and Trauma. 2011; 25 (5):377–391. [Google Scholar]
2. Kawamoto K, Kim WC, Tsuchida Y, Tsuji Y, Fujioka M, Horii M, et al. Incidence of physeal injuries in Japanese children. Journal of Pediatric Orthopedics Part B. 2006; 15 (2):126–130. [PubMed] [Google Scholar]
3. Mann DC, Rajmaira S. Distribution of physeal and nonphyseal fractures in 2650 long-bone fractures in children aged 0–16 years. Journal of Pediatric Orthopedics. 1990; 10 (6):713–716. [PubMed] [Google Scholar]
4. Bright RW, Burstein AH, Elmore SM. Epiphyseal-plate cartilage. A biomechanical and histological analysis of failure modes. Journal of Bone and Joint Surgery America. 1974; 56 (4):688–703. [PubMed] [Google Scholar]
5. Rennie L, Court-Brown CM, Mok JYQ, Beattie TF. The epidemiology of fractures in children. Injury. 2007; 38 (8):913–922. [PubMed] [Google Scholar]
6. Ogden JA. Skeletal injury in the child. 3. New York: Springer; 2000. [Google Scholar]7. Ogden JA. Injury to the growth mechanisms of the immature skeleton. Skeletal Radiology. 1981; 6 (4):237–253. [PubMed] [Google Scholar]
8. Byers PD, Brown RA. Cell columns in articular cartilage physes questioned: a review. Osteoarthritis Cartilage. 2006; 14 (1):3–12. [PubMed] [Google Scholar]
9. Peterson HA. Epiphyseal growth plate fractures. 2007. Berlin: Springer; 2007. [Google Scholar]10. Langenskiöld A. Role of the ossification groove of Ranvier in normal and pathologic bone growth: a review. Journal of Pediatric Orthopedics. 1998; 18 (2):173–177. [PubMed] [Google Scholar]
11. Moen CT, Pelker RR. Biomechanical and histological correlations in growth plate failure. Journal of Pediatric Orthopedics. 1984; 4 (2):180–184. [PubMed] [Google Scholar]
12. Dale GG, Harris WR. Prognosis of epiphyseal separation: an experimental study. Journal of Bone and Joint Surgery British. 1958; 40 (116):22. [PubMed] [Google Scholar]
13. Trueta J, Morgan JD. The vascular contribution to osteogenesis: I. Studies by the injection method. Journal of Bone and Joint Surgery British Volume. 1960; 42 (1):97–109. [PubMed] [Google Scholar]
14. Salter RB, Harris WR. Injuries involving the epiphyseal plate. Journal of Bone and Joint Surgery American Volume. 1963; 45 (3):587–622. [Google Scholar]
15. Rang M.The growth plate and its disorders.Edinburgh: E. & S. Livingstone Ltd; 1969, pp. 204. 10.1002/bjs.1800560629
16. Gufler H, Schulze CG, Wagner S, Baumbach L. MRI for occult physeal fracture detection in children and adolescents. Acta Radiologica. 2013; 54 (4):467–472. [PubMed] [Google Scholar]
17. Waters PM, Beaty J, Kasser J. Elbow, “TRASH” (the radiographic appearance seemed harmless) lesions. Journal of Pediatric Orthopedics. 2010; 30 :S77–81. [Google Scholar]
18. Rathjen KE, Birch JG. Physeal injuries and growth disturbances. 6. Philadelphia: Lippincott Williams & Wilkins; 2006. pp. 99–131. [Google Scholar]
19. Boutis K, Narayanan UG, Dong FF, Mackenzie H, Yan H, Chew D, et al. Magnetic resonance imaging of clinically suspected Salter–Harris I fracture of the distal fibula. Injury. 2010; 41 :852–856. [PubMed] [Google Scholar]
20. Carey J, Spence L, Blickman H, Eustace S. MRI of pediatric growth plate injury: correlation with plain film radiographs and clinical outcome. Skeletal Radiology. 1998; 27 :250–255. [PubMed] [Google Scholar]
21. Havránek P, Lízler J. Magnetic resonance imaging in the evaluation of partial growth arrest after physeal injuries in children. J Bone Joint Surg Am. 1991; 73 (8):1234–1241. [PubMed] [Google Scholar]
22. Parikh SN, Wells L, Mehlman CT, Scherl SA. Management of fractures in adolescents. Instructional Course Lectures. 2011; 60 :397–411. [PubMed] [Google Scholar]
23. Eismann EA, Stephan ZA, Mehlman CT, Denning J, Mehlman T, Parikh SN. pediatric triplane ankle fractures: Impact of radiographs and computed tomography on fracture classification and treatment planning. Journal of Bone and Joint Surgery American Volume. 2015; 97 (12):995–1002. [PubMed] [Google Scholar]
24. Thawrani D, Kuester V, Gabos PG, Kruse RW, Littleton AG, Rogers KJ, et al. Reliability and necessity of computerized tomography in distal tibial physeal injuries. Journal of Pediatric Orthopedics. 2011; 31 (7):745–750. [PubMed] [Google Scholar]
25. Wuerz TH, Gurd DP. Pediatric physeal ankle fracture. Journal of the American Academy of Orthopaedic Surgeons. 2013; 21 (4):234–244. [PubMed] [Google Scholar]
26. Vorhies JS, Funk S, Elliott M, Riccio A, Ramo B. The utility of intraoperative arthrogram in the management of pediatric lateral condyle fractures of the humerus. Orthopedics. 2020; 43 (1):30–35. [PubMed] [Google Scholar]
27. Escott BG, Kelley SP. Management of traumatic physeal growth arrest. Orthopaedics and Trauma. 2012; 26 (3):200–211. [Google Scholar]
28. Young JWR, Bright RW, Whitley NO. Computed tomography in the evaluation of partial growth plate arrest in children. Skeletal Radiology. 1986; 15 (7):530–535. [PubMed] [Google Scholar]
29. Lurie B, Koff MF, Shah P, Feldmann EJ, Amacker N, Downey-Zayas T, et al. Three-dimensional magnetic resonance imaging of physeal injury: reliability and clinical utility. Journal of Pediatric Orthopedics. 2014; 34 (3):239–245. [PubMed] [Google Scholar]
30. Foster BK, John B, Hasler C. Free fat interpositional graft in acute physeal injuries: The anticipatory Langenski old procedure. Journal of Pediatric Orthopedics. 2000; 20 :282–285. [PubMed] [Google Scholar]
31. Langenskiöld A. The possibilities of eliminating premature partial closure of an epiphyseal plate caused by trauma or disease. Acta Orthopaedica Scandinavica. 1967; 38 (1–4):267–279. [Google Scholar]
32. Lee TM, Mehlman CT. Hyphenated history: Park–Harris growth arrest lines. American Journal of Orthopedics (Belle Mead NJ). 2003; 32 (8):408–411. [PubMed] [Google Scholar]
33. Ogden JA. Growth slowdown and arrest lines. Journal of Pediatric Orthopedics. 1984; 4 (4):409–415. [PubMed] [Google Scholar]
34. Sferopoulos NK. Classification of distal radius physeal fractures not included in the Salter–Harris system. Open Orthopaedics Journal. 2014; 8 :219–224. [PMC free article] [PubMed] [Google Scholar]
35. Russo F, Moor MA, Mubarak SJ, Pennock AT. Salter–Harris II fractures of the distal tibia: Does surgical management reduce the risk of premature physeal closure? Journal of Pediatric Orthopedics. 2013; 33 (5):524–529. [PubMed] [Google Scholar]
36. Cain M, Stephenson M, Umapathysivam K, Williams N, Ianunzio J. Effectiveness of different minimally invasive epiphysiodesis techniques in the management of pediatric leg length discrepancies: a systematic review protocol: A systematic review protocol. JBI Database of Systematic Reviews and Implementation Reports. 2016; 14 (12):14–24. [PubMed] [Google Scholar]
37. Lee SC, Shim JS, Seo SW, Lim KS, Ko KR. The accuracy of current methods in determining the timing of epiphysiodesis. Bone and Joint Journal. 2013; 95 (7):993–1000. [PubMed] [Google Scholar]
38. Paley D, Bhave A, Herzenberg JE, Bowen JR. Multiplier method for predicting limb-length discrepancy. Journal of Bone and Joint Surgery American Volume. 2000; 82 (10):1432–1446. [PubMed] [Google Scholar]
39. Campbell CJ, Grisolia A, Zanconato G. The effects produced in the cartilaginous epiphyseal plate of immature dogs by experimental surgical traumata. Journal of Bone and Joint Surgery American Volume. 1959; 41 :1221–1242. [PubMed] [Google Scholar]
40. Garces GL, Guerado-Parra E. Modifications of growth plates after pinning. Medical Science Research. 1987; 15 :561–562. [Google Scholar]
41. Boyden EM, Peterson HA. Partial premature closure of the distal radial physis associated with Kirschner wire fixation. Orthopedics. 1991; 14 (5):585–588. [PubMed] [Google Scholar]
42. Smith JT, Kasser WPM. The effect of pinning across the physis for stabilization of fractures in children: an MRI evaluation. Orthopaedic Journal at Harvard Medical School. 2008; 10 :99–102. [Google Scholar]
43. Janus GJ, Vanpaemel LA, Engelbert RH, Pruijs HE. Complications of the Bailey–Dubow elongating nail in osteogenesis imperfecta: 34 children with 110 nails. Journal of Pediatric Orthopedics Part B. 1999; 8 (3):203–207. [PubMed] [Google Scholar]
44. Jerosch J, Mazzotti I, Tomasevic M. Complications after treatment of patients with osteogenic imperfecta with a Bailey–Dubow rod. Archives of Orthopaedic and Trauma Surgery. 1998; 117 :240–245. [PubMed] [Google Scholar]
45. Gönzalez-Herranz P, Burgos-Flores J, Rapariz JM, Lopez-Mondejar JA, Ocete JG, Amaya S. Intramedullary nailing of the femur in children: Effects on its proximal end. Journal of Bone and Joint Surgery. 1995; 77B (2):262–266. [PubMed] [Google Scholar]
46. Tan L, Sun D-H, Yu T, Wang L, Zhu D, Li Y-H. Death due to intra-aortic migration of Kirschner wire from the clavicle: A case report and review of the literature. Medicine (Baltimore). 2016; 95 (21):e3741. [PMC free article] [PubMed] [Google Scholar]
47. Langenskiöld A. Osseous bridging of the growth plate. In: Uhthoff HK, Wiley JJ, editors. Behavior of the growth plate. New York: Raven Press; 1988. pp. 259–261. [Google Scholar]
48. Langenskiöld A. Traumatic premature closure of the distal tibial epiphyseal plate. Acta Orthopaedica Scandinavica. 1967; 38 (4):520–531. [PubMed] [Google Scholar]
49. Nordentoft EL. Experimental epiphyseal injuries: Grading of traumas and attempts at treating traumatic epiphyseal arrest in animals. Acta Orthopaedica Scandinavica. 1969; 40 (2):176–192. [PubMed] [Google Scholar]
50. Janarv PM, Wikström B, Hirsch G. The influence of transphyseal drilling and tendon grafting on bone growth: an experimental study in the rabbit. Journal of Pediatric Orthopedics. 1998; 18 (2):149–154. [PubMed] [Google Scholar]
51. Makela EA, Vainionpaa S, Vihtonen K, Mero M, Rokkanen P. The effect of trauma to the lower femoral epiphyseal plate. An experimental study in rabbits. Journal of Bone and Joint Surgery British Volume. 1988; 70 (2):187–191. [PubMed] [Google Scholar]
52. Langenskiöld A, Heikel HV, Nevalainen T, Osterman K, Videman T. Regeneration of the growth plate. Acta Anat (Basel). 1989; 134 (2):113–123. [PubMed] [Google Scholar]
53. Bostock SH, Peach BG. Spontaneous resolution of an osseous bridge affecting the distal tibial epiphysis. Journal of Bone and Joint Surgery British Volume. 1996; 78 (4):662–663. [PubMed] [Google Scholar]
54. Chadwick CJ. Spontaneous resolution of varus deformity at the ankle following adduction injury of the distal tibial epiphysis. A case report. Journal of Bone and Joint Surgery American Volume. 1982; 64 (5):774–776. [PubMed] [Google Scholar]
55. Herring JA, Birch J. Whither the bar. Journal of Pediatric Orthopaedics. 1987; 7 (6):722–725. [PubMed] [Google Scholar]
56. Katz JF. Spontaneous correction of angulational deformity of the proximal femoral epiphysis after cervical and trochanteric fracture. Journal of Pediatric Orthopedics. 1983; 3 (2):231–234. [PubMed] [Google Scholar]
57. Laor T, Hartman AL, Jaramillo D. Local physeal widening on MR imaging: an incidental finding suggesting prior metaphyseal insult. Pediatric Radiology. 1997; 27 (8):654–662. [PubMed] [Google Scholar]
58. Khoshhal KI, Kiefer GN. Physeal bridge resection. Journal of the American Academy of Orthopaedic Surgeons. 2005; 13 (1):47–58. [PubMed] [Google Scholar]
59. Abbo O, Accadbled F, Laffosse J-M, De Gauzy JS. Reconstruction and anticipatory Langenskiöld procedure in traumatic defect of tibial medial malleolus with type 6 physeal fracture. Journal of Pediatric Orthopedics Part B. 2012; 21 (5):434–438. [PubMed] [Google Scholar]
60. Langenskiöld A. An operation for partial closure of an epiphysial plate in children, and its experimental basis. Journal of Bone and Joint Surgery British Volume. 1975; 57 (3):325–330. [PubMed] [Google Scholar]
61. Langenskiöld A. Bridge resection and interposition of substances. Mapfre Medicine. 1993; 4 (22):222–223. [Google Scholar]
62. Visser JD, Nielsen HK. Case report: Operative correction of abnormal central epiphyseal plate closure by transmetaphyseal bone-bridge resection and implantation of fat. The Netherlands Journal of Surgery. 1981; 33 (3):140–145. [PubMed] [Google Scholar]
63. Apte SS, Kenwright J. Physeal distraction and cell proliferation in the growth plate. Journal of Bone and Joint Surgery British Volume. 1994; 76 (5):837–843. [PubMed] [Google Scholar]
64. Robinson RG, Macalister AD. Acrylic cranioplasty: a simple one-stage method using a cold curing material. Br J Surg. 1954; 42 (173):312–315. [PubMed] [Google Scholar]
65. Rousou J, Levitsky S, Gonzalez-Lavin L, Cosgrove D, Magilligan D, Weldon C, et al. Randomized clinical trial of fibrin sealant in patients undergoing resternotomy or reoperation after cardiac operations. A multicenter study. Journal of Thoracic Cardiovascular Surgery. 1989; 97 (2):194–203. [PubMed] [Google Scholar]
66. Jie Q, Hu Y, Yang L, Lei W, Zhao L, Lv R, et al. Prevention of growth arrest by fibrin interposition into physeal injury. Journal of Pediatric Orthopedics Part B. 2010; 19 (2):201–206. [PubMed] [Google Scholar]
67. Abood AA, Møller-Madsen B, Shiguetomi-Medina JM, Stødkilde-Jørgensen H, Foldager C, Rahbek O. Autologous cartilage and fibrin sealant may be superior to conventional fat grafting in preventing physeal bone bridge formation—a pilot study in porcines. Journal of Children’s Orthopaedics. 2020; 14 (5):459–465. [PMC free article] [PubMed] [Google Scholar]
68. De Bastiani G, Aldegheri R, Renzi Brivio L, Trivella G. Chondrodiatasis-controlled symmetrical distraction of the epiphyseal plate: Limb lengthening in children. Journal of Bone and Joint Surgery. 1986; 68B :550–555. [PubMed] [Google Scholar]
69. De Bastiani G, Aldegheri R, Renzi Brivio L, Trivella G. Limb lengthening by distraction of the epiphyseal plate: A comparison of two techniques in the rabbit. Journal of Bone and Joint Surgery. 1986; 68B :545–549. [PubMed] [Google Scholar]
70. Elmer EB, Ehrlich MG, Zaleske DJ, Polsky C, Mankin HJ. Chondrodiatasis in rabbits: a study of the effect of transphyseal bone lengthening on cell division, synthetic function, and microcirculation in the growth plate. Journal of Pediatric Orthopedics. 1992; 12 (2):181–190. [PubMed] [Google Scholar]
71. Aldegheri R, Trivella G, Lavini F. Epiphyseal distraction hemichondrodiatasis. Clinical Orthopaedics and Related Research. 1989; 241 :128–136. [PubMed] [Google Scholar]
72. Canadell J, de Pablos J. Correction of angular deformities by physeal distraction. Clinical Orthopaedics and Related Research. 1992; 283 :98–105. [PubMed] [Google Scholar]
73. Bollini G, Tallet JM, Jacquermier M, Bouyala JM. Case report: New procedure to remove a centrally located bar. Journal of Pediatric Orthopedics. 1990; 10 :662–666. [PubMed] [Google Scholar]
74. Bjerkreim I. Limb lengthening by physeal distraction. Acta Orthopaedica Scandinavica. 1989; 60 (2):140–142. [PubMed] [Google Scholar]
75. Zarzycki D, Tesiorowski M, Zarzycka M, Kacki W, Jasiewicz B. Long-term results of lower limb lengthening by physeal distraction. Journal of Pediatric Orthopedics. 2002; 22 (3):367–370. [PubMed] [Google Scholar]
76. Mayr JM, Pierer GR, Linhart WE. Reconstruction of part of the distal tibial growth plate with an autologous graft from the iliac crest. Journal of Bone and Joint Surgery British Volume. 2000; 82 (4):558–560. [PubMed] [Google Scholar]
77. Gigante C, Martinez AIC. Desepiphysiodesis and reconstruction of the distal radial growth plate with an autologous iliac crest cartilage graft: A case report and review of literature. Journal of Orthopaedic Case Reports. 2019; 10 (1):70–73. [PMC free article] [PubMed] [Google Scholar]
78. Ehrlich MG. The biology of growth plate transfers (abstract) Journal of Pediatric Orthopedics. 1986; 6 :731–745. [Google Scholar]
79. Ehrlich MG, Zaleske DJ, Lalanandham T, Mankin HJ. In: Biology of growth plate transfers. Uhthoff HK, Wiley JJ, editors. New York: Raven Press; 1988. pp. 61–64. [Google Scholar]
80. Harris WR, Martin R, Tile M. Transplantation of epiphyseal plates. An experimental study. Journal of Bone and Joint Surg American Volume. 1965; 47 :897–914. [PubMed] [Google Scholar]
81. Boyer MI, Gilday D, Kiral A, Nolan L, Bowen CV. Can quantitative 99mTc-MDP bone scans be used to predict longitudinal growth of epiphyseal plate allografts after microvascular transplantation? An experimental study. Microsurgery. 1995; 16 (3):155–160. [PubMed] [Google Scholar]
82. Lee EH, Chen F, Chan J, Bose K. Treatment of growth arrest by transfer of cultured chondrocytes into physeal defects. Journal of Pediatric Orthopedics. 1998; 18 (2):155–160. [PubMed] [Google Scholar]
83. Foster BK, Hansen AL, Gibson GJ, Hopwood JJ, Binns GF, Wiebkin OW. Reimplantation of growth plate chondrocytes into growth plate defects in sheep. Journal of Orthopaedic Research. 1990; 8 (4):555–564. [PubMed] [Google Scholar]
84. Hui JHP, Li L, Teo Y-H, Ouyang H-W, Lee E-H. Comparative study of the ability of mesenchymal stem cells derived from bone marrow, periosteum, and adipose tissue in treatment of partial growth arrest in rabbit. Tissue Engineering. 2005; 11 (5–6):904–912. [PubMed] [Google Scholar]
85. Sundararaj SKC, Cieply RD, Gupta G, Milbrandt TA, Puleo DA. Treatment of growth plate injury using IGF-I-loaded PLGA scaffolds: Treatment of growth plate injury using IGF-I-loaded PLGA scaffolds. Journal of Tissue Engineering and Regenerative Medicine. 2015; 9 (12):E202–E209. [PubMed] [Google Scholar]
86. Chung R, Foster BK, Xian CJ. The potential role of VEGF-induced vascularisation in the bony repair of injured growth plate cartilage. Journal of Endocrinology. 2014; 221 (1):63–75. [PubMed] [Google Scholar]
87. Macsai CE, Georgiou KR, Foster BK, Zannettino ACW, Xian CJ. Microarray expression analysis of genes and pathways involved in growth plate cartilage injury responses and bony repair. Bone. 2012; 50 (5):1081–1091. [PubMed] [Google Scholar]
Articles from Indian Journal of Orthopaedics are provided here courtesy of Indian Orthopaedic Association