Management of Bony Defects in Revision Total Knee Joint Replacement

Shankar Thiagarajah, MB ChB, FRCS (Tr&Orth), PhD

Allan E. Gross, MD, FRCSC, O.Ont

David Backstein, MD, MEd, FRCSC

Surgeons treating patients requiring revision total knee arthroplasty (TKA) commonly encounter bone stock deficiencies. Massive bone loss occurs as a result of several etiologies including osteolysis, septic loosening, stress shielding, aberrant intraoperative bone cuts, trauma, and iatrogenic bone loss when removing well-fixed components.

The management of bone defects is dependent upon several factors including their size, location, and whether they are contained or uncontained. The key to any successful strategy is achieving implant support and stable fixation. Small contained and uncontained defects may be amenable to repair with bone cement, morselized bone graft, or modular augments. The latter are an integral part of most contemporary knee revision systems. Moderate defects may be addressed using structural allografts, modular augments, or metaphyseal fixation devices (sleeves and cones). In the face of massive uncontained metaphyseal bone loss, particularly with damage to the adjacent collateral ligaments, allograft-prosthetic composites (APCs), or more commonly megaprostheses are credible options.

In this chapter, we present the classification of bony defects in revision TKA, review the pathogenesis of bone destruction, appraise the treatment options for bony defects, outline the techniques for the treatment of bone loss, and review the results of these treatment options.

CLASSIFICATIONS

Bone defects encountered in revision TKA have been classified to enable the surgeon to categorize the extent of the bone loss. Bone defects are better assessed once all components have been removed and preliminary cuts performed intraoperatively. Classifications aid the surgeon in deciding the appropriate revision procedure and the necessary implants required.

While there is no universally accepted classification system, the most widely adopted is the Anderson Orthopaedic Research Institute (AORI) classification that provides an algorithm for the surgeon in the management of bone loss (Table 69-1).¹ Type 1 bone defects are minor contained deficiencies of trabecular bone involving the bone-implant interface. The adjacent metaphyseal bone is intact, and thus, the joint line is typically maintained. Such defects may be resected with a thicker bone cut or filled with bone graft or cement. A type 2 defect has a damaged metaphysis in either (2A) or both (2B) the medial and lateral compartments. A type 3 defect represents significant deficiencies to the metaphyseal portions of the femur and/or tibia that may involve the collateral ligaments and/or the patella tendon also. Small type 2 defects can be treated with cement, morselized graft, or metal augments. More substantial metaphyseal type 2 and type 3 defects will require structural allograft or a metaphyseal fixation device. Type 3 defects involving the adjacent ligaments will require either an APC or more commonly a megaprosthesis.

An alternative, the Mount Sinai Toronto system, considers defects simply as either contained or uncontained (segmental or circumferential) (Table 69-2).² Contained defects possess an intact circumferential cortex, whereas an uncontained defect is deficient of adequate surrounding cortical bone to allow packing it with morselized bone graft.

Contained defects are subdivided into:

Type I defects, the metaphyseal bone is intact and no bone grafting or augmentation is required to restore a normal joint line. Small bone defects can be filled with cement or resected with a bone cut. While not always absolutely necessary, generally a stemmed, condylar prosthesis is recommended to be used in all revision TKA cases.

Type II defects have damaged metaphyseal bone. Small defects (<1.5 cm) may require bone grafting, a cement fill, or metal augments to restore a normal joint line. These defects are best treated with stemmed revision prostheses, particularly when augments are deployed. Larger defects will require a structural allograft or a metaphyseal fixation device (sleeve or cone).

TABLE 69-1 Anderson Orthopedic Research Institute (AORI) Classification of Bone Loss for the Distal Femur and Proximal Tibia

AORI Grade (Femur)	Defect	MCL/LCL	Bone Reconstruction Options
F1	Intact metaphyseal bone	Intact	Cement or morselized graft
F2a	Metaphyseal loss, single condyle	Intact	Metal augment or allograft
F2b	Metaphyseal loss, both condyles	Intact	Structural graft or metaphyseal fixation device
F3^a	Deficient metaphysis	Compromised	Allograft-prosthetic composite or megaprosthesis
AORI Grade (Tibia)	Defect	MCL/LCL	Bone Reconstruction Options
T1	Intact metaphyseal bone	Intact	Cement or morselized graft
T2a	Metaphyseal loss, single plateau	Intact	Metal augment or allograft
T2b	Metaphyseal loss and lateral plateau	Intact	Metal augment, structural graft, or metaphyseal fixation device
T3^a	Deficient metaphysis	Compromised	APC or segmental replacement
^aPossible extensor mechanism compromise.
LCL, lateral collateral ligament; MCL, medial collateral ligament.

Uncontained defects have segmental bone_, loss with no remaining cortex. These defects are subdivided as:

Type III or noncircumferential defects. Small defects may be addressed using a structural allograft and/or modular augments, whereas larger deficiencies will require a structural allograft or a metaphyseal fixation device.

Type IV or circumferential defects. Massive defects involving the collateral ligaments require a megaprosthesis or APC.

PATHOGENESIS OF BONE DEFECTS IN TOTAL KNEE REPLACEMENT

The etiology of bony defects is multifactorial. In this section, we discuss mechanical bone loss, stress shielding, osteolysis, and infection.

Mechanical Bone Loss

Historically, bone excision at the time of the primary TKA was a common cause of bone loss. Due to the excessive constraints in many early designs, high rotational forces were distributed to the implant-bone interface, which led to premature loosening of the implant. Gross loosening resulted in a windshield-wiper-like action, often with dramatic bone loss.³,⁴ The early 1980s witnessed a transition to resurfacing-style prostheses requiring minimal bone resection and using relatively thin polyethylene inserts. Paradoxically, this resulted in increased polyethylene wear, which led to particulate-mediated osteolysis.⁵,⁶,⁷,⁸

Iatrogenic bone loss can occur at the revision of well-fixed components, particularly in the case of cementless implants. The posterior femoral condyles are particularly at risk. Thus, great care must be taken to ensure that the bone-cement-implant interface is loosened adequately before implant removal.

Stress Shielding

The tibial component is the most common implant to fail in TKA surgery due to compressive failure of trabecular support.⁹ Stress shielding may be an important factor in this mechanism of failure. Use of a metal tibial tray and stem has been shown to reduce maximum compressive stresses in underlying bone by up to 39%.¹⁰

The strength of the metaphyseal region of the distal femur is also reduced. Finite element analysis reveals that the rigid femoral component reduces stress to the anterior distal femur by a magnitude of 1.¹¹ Bone loss occurs primarily in the first year, however, can progress thereafter.¹² The effect of the type of fixation on stress shielding is controversial. Mintzer et al¹³ showed that osteopenia was independent of implant design and fixation, whereas Seki et al¹⁴ demonstrated a 57% decrease in bone density with a cemented implant compared with a 28% drop for a cementless implant of the same design. This area of stress shielding correlates with the clinically and radiographically observed area of osteopenia in the anterior distal femur.

Osteolysis

Wear particle generation is a significant factor in stimulating periprosthetic inflammation and subsequent bone loss in total joint arthroplasty.¹⁵ Historically, osteolysis was common in TKA and could occur in the femur, tibia, and patella. Osteolysis would result in catastrophic failure of the construct when the bone is unable to support the implant.⁹,¹⁶ Weakening of the subchondral bone could also lead to periprosthetic fractures.¹⁷,¹⁸

The etiology of wear particle generation is multifactorial. Finite element analysis has demonstrated much higher
contact stresses in the nonconforming TKA than in the more conforming total hip arthroplasty.⁵,¹⁹,²⁰ Clinically, this is demonstrated from retrievals of tibial polyethylene inserts in less conforming TKAs.⁵,⁶,⁸,²¹ Contact stresses in TKA can exceed the yield stress of polyethylene, particularly if the polyethylene is less than 6 mm. The nonarticulating surface of the polyethylene can also generate wear particles.²²,²³ This has been termed back-sided wear. Studies by Engh et al²² demonstrated a wide variation in the degree of wear between implants. Wear characteristics of the inner tray surface and integrity of the tibial implant locking mechanism are important factors.

TABLE 69-2 Mount Sinai Classification of Bone Loss at the Knee

Type	Type of Bone Loss	Description	MCL/LCL	Bone Reconstruction Options
1	No notable loss of bone stock	There may be erosion of the endosteal bone, but no involvement of the cortex. No migration of the primary component has occurred, and bone is largely intact.	Intact	Cement or morselized graft
2	Contained loss of bone stock with cortical thinning	The canal is widened, but there still exists a sleeve of cortical bone.	Intact	Cement if <4 mm Metal augment if 4-15 mm Metaphyseal fixation device or structural allograft if >15 mm
3	Uncontained (segmental) loss of bone stock >50% of medial and/or lateral condyle	Uncontained bone loss represents less than 50% of the medial and/or lateral femoral and/or tibial condyle and is less than 15 mm in depth.	Intact	Metal augment if unicondylar Metaphyseal fixation device or structural allograft if involving both condyles
4	Uncontained (segmental) loss of bone stock >50% of medial and/or lateral condyle	Uncontained bone loss represents greater than 50% of the medial and/or lateral femoral and/or tibial condyle and is greater than 15 mm in depth.	Deficient	Megaprosthesis or APC
APC, allograft-prosthetic composite.

The numbers of wear particles increases with applied load and number of cycles. Thus, greater osteolysis is expected in heavier and more active patients.²⁰,²⁴,²⁵ Limb malalignment causing increased contact stresses increases both wear and mechanical collapse, potentially leading to premature failure.²⁶ The polyethylene patella button is also a source of wear particles. The force across the patellofemoral joint can be in excess of 4600 N. This can be over a small area, particularly if there is patella maltracking or tilt.²⁷ Thus, the yield strength of polyethylene may be exceeded.²¹

Material-related causes of osteolysis include the use of poor-quality polyethylene,⁷,²¹ heat-pressed polyethylene,²¹,²⁸ or gamma-irradiated polyethylene, which oxidizes²⁹; the use of titanium as a bearing surface³⁰,³¹,³²; and screw fixation of tibial implants.³³ Some reports suggest that osteolysis is more common with cementless implants.²⁴,³⁴ Extensive porous coating has been shown to decrease the incidence of osteolysis.³⁵ While highly cross-linked polyethylene has been reported to be as an effective material for decreasing polyethylene wear and osteolysis in TKA, this has not yet been shown to improve the clinical and radiographic outcomes in mid-term follow-up after TKA.³⁶ While relatively recently adopted, highly cross-linked polyethylene has contributed to a rapid decline in revision rates due to osteolysis. Consequently large bony defects secondary to polyethylene wear-associated osteolysis are now seldom encountered.

Infection

Infection causes an acute inflammatory reaction and the production of a purulent cytokine-rich inflammatory exudate that can result in rapid destructive bone loss. Low-virulence organisms such as Staphylococcus epidermidis can result in progressive periprosthetic radiolucencies without frank clinical signs of infection.

Further bone loss can occur at the time of implant removal during revision of an infected TKA. The
two-stage revision approach may also lead to further mechanical bone loss from compression and abrasion due to the use of antibiotic spacers. One study quantified the loss as an average of 12.8 mm for the femur and 6.2 mm for the tibia.³⁷ No metal rods were inserted across the knee. The authors will typically use a poorly cemented condylar total knee prosthesis at the first stage if stability of the knee permits its use. If the knee is unstable (e.g., the medial collateral ligament is deficient), then either a cemented rotating hinged prosthesis or a tibial intramedullary nail is used to bridge the knee.

TREATMENT

Options

Commonly accepted options for the treatment of bony defects in revision TKA include bone cement, autograft, structural allograft, modular augmentation, metaphyseal fixation devices, megaprostheses, and APCs. The technique used depends on the degree of bone loss and the extent to which the defect is contained.

Bone Cement

Cement has a role in filling contained defects where the bone loss is minimal. The major advantage of bone cement is that it can be molded to fit an irregular defect. It is a nonphysiologic material, however, and therefore lacks biomechanical integrity in larger defects, even when used with screws. The author’s indications for use of cement alone are therefore limited to cases with an uncontained defect which is less than 5 mm in depth. For contained defects with a solid surrounding rim of the bone, cement may be used when the deficiency involves less than 50% of the hemi tibial plateau or femoral condyle.³⁶

Autograft

Autograft is the optimum material for grafting defects, as it is both osteoinductive and osteoconductive. However, bony defects are often too large to be repaired solely with autograft. It is the authors’ experience that contained defects greater than 10 mm × 10 mm are difficult to fill with autologous bone alone, and generally speaking, autologous bone is not an option for contained defects in the revision context. Despite this, autograft is useful to augment and enhance allograft in contained defects, and its use is imperative at the host-allograft interface to ensure healing.

Allograft

Allograft is an appealing alternative to autograft as it also restores bone stock. It is available in unlimited quantities, and there is no donor site morbidity. While the graft can be tailored to match the geometry of the bony defect, the use of allograft size matching with the dimensions of the defect is advantageous as any modification of the original allograft may theoretically weaken it. Allograft is osteoconductive but not osteoinductive; thus, the incorporation of cancellous bone and the healing of cortical bone are slower than with autogenous grafts.³⁸ Allograft incorporation varies with the clinical scenario. The most critical factor is the recipient host bed. Morselized allograft incorporation occurs through a combination of revascularization, osteoconduction, and remodeling. In contrast, a structural allograft unites to the host at the host-allograft interface, but there is limited internal remodeling of the allograft.³⁹ A structural allograft is defined as any allograft not composed of morselized bone that is used to fill a defect.² Revision TKA with structural allograft typically makes use of femoral heads, bulk tibia, or bulk distal femoral and proximal tibial allografts to achieve mechanical stability for the implants.

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