The introduction of a new implant material is not without risk. A series of worst-case scenarios were developed and tested accordingly to answer questions such as: what will happen if the implant is not placed in a good orientation? What will happen to the material after a long implantation time, e.g. 20 or more years?

To reach a higher level of safety, a new approach for the preclinical testing has been taken. The vitamys® material (a novel vitamin-doped HXLPE) followed a severe pre-clinical testing protocol, including mechanical, tribological and biocompatibility testing. The testing includes a comparison of vitamys® vs. standard-UHMWPE and other HXLPE after accelerated ageing for periods equivalent to 20 and 40 years in-vivo. Hip simulator testing was done at inclination angles from 35° to 65° to assess the “forgiveness” of the material for mal-orientation.

Comparing the test results to published data, it becomes evident that the vitamin addition and the sequence of the manufacturing steps both have a significant effect of the resulting mechanical, ageing and wear properties. In contrast to UHMWPE or HXLPE without antioxidant, the vitamys material behaves in a very “forgiving” manner: Hip simulator testing of vitamys at high inclination angles and even with severely aged material revealed no increase of wear rates. The vitamys material was first introduced in a monoblock polyethylene cup with a thin Ti-particle coating, the RM-Pressfit vitamys® acetabular cup (Mathys Ltd Bettlach, Switzerland). Its first implantation occurred in Sept. 2009. Since then, a total of nearly 500 implantations have been documented in a prospective multi-centre clinical study involving 11 clinics in 5 countries (CH, DE, FR, NL and NZ).

Based on the pre-clinical testing and its first clinical experience, we have reason to believe that the RM-Pressfit vitamys® possesses interesting and unique features such as high elasticity (no stress-shielding), high ageing and wear resistance combined with clinically proven biological anchorage – making it theoretically suitable for a whole range of patients, including the young and active.

We present our mid-term results with the use of structural allografts in cases of revision of failed THA due to infection.

Eighteen patients with a deep infection at the site of a THA were treated with a two-stage revision, which included reconstruction with massive allografts. All the allografts were frozen and sterilised by gamma-irradiation. The mean age at the time of the revision was 65.9 years. A cement spacer containing 1 g of Gentamicin was used during the interval period. Parenteral antibiotics were administrated for a period of three to four weeks. Oral antibiotics were given for an average of 18 weeks. The patients were followed for a mean of 8.9 years (5.4–14.2).

Definite deep wound infection developed in one patient (5.6%), who underwent resection arthroplasty. An additional patient underwent re-revision of an acetabular component for mechanical loosening. The mean HHS improved from 34.2 points preoperatively to 70.7 points at the last review. Sixteen of the patients (88.9%) had a successful outcome. Kaplan-Meier survivorship analysis predicted 80.95% rate of survival at 14 years.

Radiographicly, all allografts were found to be united to host bone. There were no signs of definite loosening of any of the implants. The complications include one fracture and two postoperative recurrent dislocations.

The use of massive allografts in a two-stage reconstruction for infected THA gives satisfactory results and should be considered in cases complicated with severe bone stock loss, where standard revision techniques are not an option.

We have followed a consecutive series of revision hip arthroplasties, performed for severe femoral bone loss using anatomic specific proximal femoral allografts

Forty-nine revision hip arthroplasties, using anatomic specific proximal femoral allografts longer than five centimetres were followed for a mean of 10.4 years.

The mean preoperative HHS improved from 42.9 points to 76.9 points postoperatively. Six hips (12.2%) were further revised, four for non-union and aseptic failure of the implant (8.2%), one for infection (2%), and one for host step-cut fracture (2%). Junctional union was observed in 44 hips (90%). Three hips underwent re-attachment of the greater trochanter for trochanteric escape (6.1%). Asymptomatic non-union of the greater trochanter was noticed in three hips (6.1%). Moderate allograft resorption was observed in five hips (10.2%). Two fractures of the host step-cut occurred (4.1%). There were four dislocations (8.2%), two of them developed in conjunction with trochanteric escape. By definition of success as increase of HHS by 20 points or more, and no need for any subsequent re-operation related to the allograft and/or the implant, a 75.5% rate of success was found. Kaplan-Meier survivorship analysis predicted 73% rate of survival at 12 years, with the need for further revision of the allograft and/or implant as the end point.

We conclude that the good medium-term results with the use of large anatomic- specific femoral allografts justify their continued use in cases of revision hip arthroplasty with severe bone stock loss.

A radiation sterilisation dose (RSD) of 25 kGy is commonly recommended for sterilisation of allograft bone. However, the mechanical and biological performance of allograft bone is gamma dose-dependent. Therefore, this study aimed to apply Method 1 – ISO 11137–2: 2006 to establish a low RSD for frozen bone allografts. Two groups of allograft bones were used: 110 femoral heads (FH) and 130 structural and morselized bones (SMB).

The method included the following stages: bioburden determination using 10 FHs and 30 SMBs; verification dose selection using table six in the ISO standard and bioburden; the verification dose was used to irradiate 100 samples from each group; then irradiated bone segments were tested for sterility. The criterion for accepting the RSD as valid is that there must be no more than two non-sterile samples out of 100. The radiation sterilisation dose is then established based on table five, ISO 11137– 2: 2006.

The bioburden of both types of frozen allograft was zero. The verification dose chosen was 1.3 kGy. Two hundred bone segments were irradiated at 1.3 kGy. The average delivery gamma dose was 1.23 kGy (with minimum dose of 1.05 kGy maximum dose of 1.41kGy), which is acceptable according to the ISO standard. Sterility tests achieved 100% sterility. Accordingly, 11 kGy was established as a valid RSD for those frozen bone allografts. A reduction in the RSD from 25 kGy to 11 kGy will significantly improve bone allograft mechanical and biological performance because our data show that this dose level improves the mechanical toughness and osteoclast activity of the allograft by more than 10 and 100 percent, respectively, compared with bone allografts irradiated at 25 kGy.

A low RSD of 11 kGy was established for allograft bones manufactured at Queensland Bone Bank by applying dose validation method 1 (ISO 11137.2-2006) that is internationally accepted.

It is not known if the radiation sterilisation dose (RSD) of 25 kGy affects mechanical properties and biocompability of allograft bone by alteration of collagen triple helix or cross-links. Our aim was to investigate the mechanical and biological performance, cross-links and degraded collagen content of irradiated bone allografts.

Human femoral shafts were sectioned into cortical bone beams (40 × 4 × 2 mm) and irradiated at 0, 5, 10, 15, 20, and 25 kGy for three-point bending tests. Corresponding cortical bone slices were used for in vitro determination of macrophage activation, osteoblast proliferation and attachment, and osteoclast formation and fusion. Subsequently, irradiated cortical bone samples were hydrolised for determination of pyridinoline (PYD), deoxypyridinoline (DPD), and pentosidine (PEN) by high performance liquid chromatography (HPLC) and collagen degradation by the alpha chymotrypsin (ï_jCT) method.

Irradiation up to 25 kGy did not affect the elastic properties of cortical bone, but the modulus of toughness was decreased from 87% to 74% of controls when the gamma dose increased from 15 to 25 kGy. Macrophages activation, the proliferation and attachment of osteoblasts on irradiated bone was not affected. Osteoclast formation and fusion were less than 40% of controls when cultured on bone irradiated at 25 kGy, and 80% at 15 kGy. Increasing radiation dose did not significantly alter the content of PYR, DPD or PEN but increased the content of denatured collagen.

Cortical allografts fragility increases at doses above 15 kGy. Decreased osteoclast viability at these doses suggests a reduction in the capacity for bone remodelling. These changes were not correlated with alterations in collagen cross-links but in degradation to the collagen secondary structure as evidenced by increased content of denatured collagen.