Aseptic Loosening of implants is caused by osteolysis. It is most significant factor limiting longevity of THA. Revision for loosening is 4x higher than next leading cause (dislocation at 13.6%), and its particularly problematic in younger patients .
Osteolysis is bone resorption caused by the body’s response to particulate debris generated as the THA implant wears out. Motion between any two components of the prosthesis (ie the femoral head and the acetabuluar liner, the head-neck junction of the femoral stem, or the liner and shell of the acetabulum) generates debris that floats around the joint. This debris stimulates a host response. Particles of metal, poly, or cement can all cause osteolysis, albeit different types of reaction. Osteolysis is important because it leads to implant loosening and/or periprosthetic fractures.
While osteolysis is the primary cause of loosening, infection must be part of the differential diagnosis.
Historical Perspective: Osteolysis was first described by Harris in 1976 and it was attributed to “cement disease” , because it was observed around the femoral component, and this was what started the drive for cementless implants. Yet after significant R&D, and development of cementless implants, osteolysis was still seen around the implants , and the histology was similar between cemented  and cementless implants . Surgeons then looked for another cause of osteolysis and recognized that it was produced by wear particles.
Stages of Osteolysis
1) Debris production (ie poly wear) is the initial stage (we talk about metal debris in a separate section because it behaves totally differently, see section). Particulate debris in THA is produced by Abrasive and Adhesive wear (whereas the TKA produces delaminating wear: small fissures form within the poly).
▪ Adhesive wear is two surfaces bonding together causing the softer material to “peel” off as a thin film onto the harder surface during motion.
Volumetric wear is a specific type of adhesive wear, and it occurs as the femoral head articulates with the cup liner, and the amount of wear is proportional to the femoral head radius squared (therefore larger femoral head = more wear..this is why the initial Charnley implants, which used conventional poly, used a size 22 femoral head). Linear wear is caused by focused stress on a isolated part of the poly due to abnormal loading.
▪ Abrasive wear occurs when a harder surface (which is never completely smooth) cuts or ploughs through a softer surface, like a cheese grater. Both cause particle formation. Most wear occurs superiorly in the cup (or at the rim in cases of impingement).
The conventional PE wear from articulating with a Cobalt-chrome head is 0.10 mm/year. The ultramolecular weight poly (UMWPE, also known as highly-crosslinked poly) wear is about 0.02 mm/year. What is the difference between conventional and UMWPE? The quality of PE depends on the consolidation of PE (the shape is formed using compression molding), the preparation (irradiation causes extensive cross-linking which decreases susceptibility to oxidation and wear), and the packaging (poly is sterilized in inert gas to prevent free-radical formation…although it can oxidize over time within the body, which is the reason some poly contains Vit. E,, which theoretically eats up the free radicals generated with oxidation)  .
The debris then travels in the joint fluid and reacts with any area of bone that is in contact with the fluid (this is an important concept when considering whether to place acetabular screws as this hardware effectively increases the surface area of bone in contact with synovial fluid…referred to as the “effective joint space” , this concept also highlights the value of circumferential porous coating in the femoral stem, because it reduces the effective joint space by causing bone ingrowth and blocking the path of joint fluid around the implant).
2) Immune Reaction & Bone Loss. Poly debris activates macrophages to initiate an inflammatory response by releasing the standard cytokines (ie TNF-alpha, RANKL, IL-6, and IL-1) that stimulate osteoclast activity, inhibit osteoblast activity, and promote progressive bone loss around the prosthesis. Osteolysis is typically progressive. Its often asymptomatic until catastrophic failure, which occurs in the form of sudden implant loosening or an acute periprosthetic fracture (due to severe bone loss, the bone breaks under minimal stress).
Because osteolysis is a chronic issue that causes acute complications, it must be monitored with serial radiographs for progressive changes every 3 to 6 months. Signs of large lytic lesions, significant progression, or loose implants are the indications for revision surgery (even in the absence of symptoms).
clinical correlate: Plain x-rays typically underestimate the size of osteolytic lesions, with lytic lesion only visible on x-ray once 20-30% of acetabular bone loss has occurred .
3) Implant Loosening. There is no universal definition of loosening. Many consider x-ray evidence (progressive radiolucency or implant migration) sufficient to diagnose loosening, while many require clinical decline to be included for diagnosis. Lets consider the clinical and radiographic signs.
clinical correlate: Loosening is considered when patients report “start-up” pain (pain with their first steps, which gradually resolves, suggesting that the implant moves, then settles into a stable position during weight bearing).
X-ray. The femur and pelvis have been divided into zones called Gruen Zones, which help to identify areas of osteolysis. The inter-oberver reliability is somewhat suspect and therefore, these zones are mainly for academic purpose and less useful clinically. In general serial x-rays are performed,and changes in implant positioning, such as stem subsidence, provides the best evidence. The accepted diagnostic criteria for loosening is progressive radiolucency or implant migration.
Radiolucent lines that progress >2 years after surgery, or new radiolucent lines over 1 mm are significant signs of loosening. Thinning is not the only sign to look for. Focal areas of high cortical density (radiopaque lines), especially around the collar or at the end of the stem, indicate non-uniform stress (ie pedestal formation at the calcar), which suggest loosening . But remember that not all cortical thinning is osteolysis (age-related thinning, or stress shielding also cause thinning). Also, in a cementless implant, a “spot weld” found at the distal end of the stem is a sign of stable fixation. In the acetabulum there are 3 zones of radiolucency, however, radiolucencies isolated to one or two zones is less specific. Leopold et al found nonprogressive lucencies in over 50% of revised components that were performing well clinically.
Migration. Femoral component migration is best evaluated by comparing the position of the stem relative to the calcar on serial x-rays. Acetabular component migration (superior or medial) should similarly be examined. A loose acetabulum may also demonstrate changes in version or inclination.
Cement Implants. In cemented implants debonding or cement fracture will precede loosening (cement implants can loosen by fatigue fracture where cracks propagate into pre-existing pores of the cement mantle). However debonding doesn’t always cause loosening. For example, a supero-lateral lucency around the stem < 2 mm does not indicate loosening. Different with cemented implants. Changes at the bone-cement interface can just be remodeling rather than loosening, however, radiolucency at the implant-cement interface is loosening. If there is rapid osteolysis or bone disintegration then be suspicious of infection.
Look for complete radiolucent line and implant migration. An incomplete radiolucent line of 50-99% implant is only possibly loose. Progressive radiolucent line around cement-bone interface is probably loose. If radiolucency is <50% is unlikely loose if nonprogressive. The loosening rates for a cemented femur are impressively low, going back to the Charnley stem, survivorship at 20 years was over 95%, at 25 years about 89% and at 30 years about 82%.
Press-Fit Implants. many demonstrate some level of subsidence from initial position, and early subsidence < 5 mm usually leads to integration without problem, and the proximal taper allows for stable fit. The acetabular component should have circumferential radiolucent line >2 mm or implant migration.
The decision to operate and the type of revision surgery is controversial. Does all osteolysis need surgery? A loose implant should be revised. Symptomatic osteolysis should be revised. But the need for surgical intervention for osteolysis around a stable implant in an asymptomatic patient is less clear. The decision to operate on a hip depends on a few variables: rate of progression (delta); location of osteolysis, type of implant, activity level and age of the patient.
Studies examining the timing for surgical intervention [12 - 15] offer some guidelines. Even a few small areas of integration can keep a cup stable and thus patients remain asymptomatic despite expansile lesions  . Yet progressive osteolysis will continue to reduce the area of integration until failure inevitably occurs. Thus, in general, lesions that progress over 3-6 month period should be revised. Femoral osteolyisis similarly remains asymptomatic until extensive synovitis occurs or impending fracture.
Femoral Implant Revision.
Osteolysis causes different degrees of bone loss. The Paprosky Classification was established to grade the severity of bone loss, which in turn guides treatment (different grades of bone loss require different implants to achieve stability).
Proxmially coated stems (primary implants) can be used if sufficient metaphyseal bone stock for ingrowth. Fully-coated stems (cylindrical monoblock) are used for deficient metaphyseal bone stock but decent diaphyseal bone (type 2, type 3A), however, there were high failure rates if used in cases with notable deficiency in diaphyseal bone stock. Fluted, Tapered Stems (Wagner-type) either monoblock or modular are successful for type 3B, and some type 4. Modular Wagner-type stems have grown in popularity because adjustments can be made if the final implant subsides more than the trial implant. Oncology prosthesis are often needed in type 4 implants when the bone stock is deficient past the isthmus of the femur.
Acetabular Implant Revision.
Asymptomatic acetabular osteolysis maybe be treated with a) implant revision or b) implant retention with bone grafting of the defect and head/liner exchange; or c) no surgery, close monitoring. Symptomatic acetabular osteolysis and gross loosening of the cup is treated with full component revision.
Similar to the femoral side, there is a Paprosky Classification for Acetabular Osteolysis, which grades the severity of bone loss and guides implant choices. Different grades of bone loss require different implants to achieve stability.
Head/liner exchange: considered if the components are well aligned . Yet despite well aligned components there is still a 10% re-revision rate for liner exchange  vs. 2% re-revision rate after the cup is revised . Yet other studies have found less significant differences in revision rates when the implants are well positioned . In cases of malpositioned components, which may be accelerating wear, complete implant revision is probably indicated.
Cup Revision: Many surgeons will fully revise a cup with significant osteolysis, but all surgeons will revise a malpositioned cup with osteolysis and any loose cup. The cup is loose if there is >2 mm of migration observed on serial x-ray, or if there are any signs of rotational changes, any screw breakage, or a radiolucent line (>1 mm) seen in all 3 zones  .
If the rim is supportive (type 1) or partially supportive (type 2 - over 2/3 rim intact, 50% contact with bone), then a standard cup can be used (consider multi-hole or high porous metal for better scratch fit). Augments or cement + rebar can be incorporated to improve stability.
Special implants (i.e. Triflange cup, or cup-cage) are needed when the rim is unsupportive (type 3) causing the implant to rock up and roll out posteriorly (type 3A) or roll up and in causing a superior medial defect (type 3b).
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