Loosening of the prosthesis

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Representation of a known septic prosthesis loosening in the FDG PET / CT

The loosening of the prosthesis is a phenomenon that occurs in approx. 8% of all implanted joint prostheses within 10 years of installation. This affects around 10,000 to 12,000 patients worldwide each year.

to form

A distinction is made between aseptic and septic loosening of the prosthesis.

The main causes of aseptic loosening of the prosthesis are :

  • Abrasion particles (e.g. made of polyethylene (PE), bone cement , ceramic or metal)
  • Lack of initial stability during implantation

In the context of septic prosthesis loosening , which is caused by minimal infections during implantation, a distinction is made:

  • high-grade infections with typical symptoms of inflammation
  • low-grade infections with atypical or no symptoms at all

therapy

In the context of loosening the prosthesis, the only thing left to maintain the patient's mobility is revision surgery with explantation of the loosened prosthesis and implantation of a replacement. During explantation, the periprosthetic membrane that forms physiologically between the prosthesis and the surrounding bone or cement is removed.

In the case of aseptic loosening of the prosthesis, the explantation and re-implantation of a new prosthesis usually take place at one time, i.e. H. during the same operation, while with infected prostheses the procedure is often "two-stage" - but a one-stage procedure is just as possible. Which method is superior and when is controversial. In the case of a two-stage procedure, after the infected prosthesis has been removed, antibiotic therapy is first carried out and materials containing antibiotics are inserted in place of the previous prosthesis (e.g. a gentamicin-containing bone cement spacer), before a revision prosthesis is implanted a few weeks later .

The prostheses that are used after loosening an initial prosthesis are so-called revision prostheses and are often significantly larger in size, since loosening is often associated with a considerable loss of bone substance. If necessary, a bone transplant to reinforce or rebuild the bony prosthesis bed must be carried out, which can be carried out autogenously from other parts of the body (e.g. cancellous plastic from the iliac crest) or allogeneically with foreign bones from a bone bank. In general, the survival time of revision prostheses is shorter than that of primary prostheses, with the risk of renewed loosening.

Using special surgical techniques (e.g. impaction grafting ), however, the defective bone bed can be reconstructed in such a way that a survival time comparable to that of the initial implantation can be expected even with largely conventional prosthesis types. In the event of septic loosening, bone grafts that have been partially impregnated with antibiotics can be used. This enables one-stage replacement operations in which, after the loosened or infected prosthesis has been removed, a new prosthesis is implanted directly as part of the same procedure, after the infection has been repaired and bone defects have been reconstructed.

Periprosthetic membrane

The periprosthetic membrane is a border of connective tissue that forms between the bone and the endoprosthesis. This membrane can also form around fixed implants and is approx. 0.1 mm thick. With loosened prostheses, however, the thickness is up to 1.0 cm. Their histological structure depends on the cause of the loosening.

In 2006, a consensus classification was used to classify the periprosthetic membrane into 4 subtypes, which arise from different causes and are related to the duration of the endoprostheses.

Consensus classification

Here, 370 periprosthetic membranes, which were removed when replacing the prosthesis, were examined histologically by pathologists using a microscope. This classification is widely recognized and used internationally. Even high-ranking journals like the New England Journal of Medicine refer to it. The classification distinguishes 4 subtypes of the periprosthetic membrane:

  • Type 1 , abrasion-induced type

Occurs in approx. 55% of the cases and is associated with an average prosthesis life of 10.1 years . The microscopic image mainly shows macrophages , which take up smaller abrasion particles, and multinucleated giant cells , which take up large particles. Leukocytes are only found sporadically. Type 1 membranes are significantly more common in cemented endoprostheses.

  • Type 2 , Infectious Type

Occurs in approx. 20% of cases and is associated with an average prosthesis service life of 3.2 years . The microscopic image shows activated fibroblasts , proliferation of small blood vessels , edema and many neutrophils , as well as accumulations of plasma cells in the low-grade infection . In the high-grade infection, neutrophils are in abundance with abundant edema. Type 2 membranes occur with about the same frequency in cemented and non-cemented endoprostheses. The bacteria causing the infection include primarily skin germs such as Staphylococcus epidermidis or the germ Staphylococcus aureus .

  • Type 3 , mixed type

Occurs in approx. 5% of the cases and is associated with an average prosthesis life of 4.5 years . The microscopic image shows properties of membrane types 1 and 2, which each occupy certain areas of the periprosthetic membrane. Type 3 membranes are a little more common in uncemented endoprostheses.

  • Type 4 , indifference type (not abrasion-induced or infectious)

Occurs in approx. 15% of the cases and is associated with an average prosthesis life of 5.4 years . The microscopic picture shows connective tissue rich in collagen , partly with fibrin coatings . The formation of a cover cell layer from fibroblasts and macrophages similar to a synovial membrane is also possible. Type 4 membranes are twice as common in uncemented endoprostheses.

In 5% of the cases it is not possible to assign the periprosthetic membrane. The consensus classification can be carried out well and reliably and has a reproducibility between several investigators of approx. 85%.

In the extended consensus classification of the periprosthetic membrane, in addition to the four types of membrane mentioned, other entities important for the pathogenesis of endoprosthesis loosening are included, which can be reliably diagnosed using histopathology and with the aid of clinical information.

The extended consensus classification includes:

  • Arthrofibrosis

The Arthrofibrosis , which may be in a wear-induced and in a non-wear-induced shape. This leads to excessive internal scarring of the joint.

  • Implant allergy

This much discussed entity is characterized by a dense, nodal-lymphatic infiltrate and appears to be due to an allergic reaction to endoprosthesis materials.

  • Osseous pathologies

In addition to the joint and neosynovial nerve, the implant-bearing bone itself can show pathological changes that lead to loosening of the prosthesis. This includes the classification of periprosthetic ossification , aseptic bone necrosis and also the fracture of the implant bed.

Validation of the consensus classification

Since 2006, the consensus classification for loosening the prosthesis has been examined and validated several times. Here new knowledge was gained:

  • In 93% of the cases, the histological consensus classification achieves the exact diagnosis of periprosthetic joint inflammation (type 2 or 3) and is therefore more precise than all other clinical methods.
  • The histological diagnosis of septic prosthesis loosening (type 2 or 3) is likely if 23 or more neutrophils can be detected per 10 high power fields (HPF).
  • The enzyme chitinase is particularly high in the blood of patients with wear-induced loosening of the prosthesis (type 1).
  • The MSF (megakaryocyte stimulating factor) gene is increasingly expressed in the periprosthetic membrane. A splice product from MSF is Lubricin , which increases the gliding ability in the physiological joint. An increased gliding ability of the periprosthetic membrane could accelerate the loosening of the prosthesis.

Individual evidence

  1. ↑ DJ Berry et al .: Twenty-five-year survivorship of two thousand consecutive primary Charnley total hip replacements: factors affecting survivorship of acetabular and femoral components. In: The Journal of Bone & Joint Surgery . 84-A, 2002, pp. 171-177. PMID 11861721 .
  2. ↑ DC Wirtz et al: Etiology, diagnosis and therapy of aseptic hip prosthesis loosening - a status assessment. In: Journal for orthopedics and their border areas. 135, 1997, pp. 270-280. PMID 9381761 .
  3. ↑ Heinz Winkler: Rationale for one stage exchange of infected hip replacement using uncemented implants and antibiotic impregnated bone graft - review . In: International Journal of Medical Sciences . Vol. 6, No. 5 , 2009, ISSN  1449-1907 , p. 247-252 , doi : 10.7150 / ijms.6.247 , PMID 19834590 (English, PDF file; 164 kB ).
  4. ^ I. Bos: Tissue reactions around loosened hip joint endoprostheses. A histological study of secondary capsules and interface membranes. In: The orthopedist. 30, 2001, pp. 881-889. PMID 11766632 .
  5. ↑ Periprosthetic membrane of loosened endoprostheses on pathologie-ccm.charite.de, (online) ; last accessed on May 21, 2012.
  6. ↑ a b c d e f L. Morawietz et al: Proposal for a histopathological consensus classification of the periprosthetic interface membrane. In: Journal of Clinical Pathology . 59, 2006, pp. 591-597. PMID 16731601 .
  7. ↑ JL Del Pozo et al: Clinical practice. Infection associated with prosthetic joints. In: N Engl J Med . 361, 2009, pp. 787-794. PMID 19692690 .
  8. ^ V. Krenn et al.: Joint endoprosthesis pathology - histopathological diagnosis and classification. In: The Pathologist. 32, 2011, pp. 210-219. PMID 21526399 .
  9. ↑ M. Mueller et al .: Histopathological diagnosis of periprosthetic joint infection following total hip arthroplasty: Use of a standardized classification system of the periprosthetic interface membrane. In: The orthopedist. 38, 2009, pp. 1087-1096. PMID 19690832 .
  10. ↑ L. Morawietz et al: Twenty-three neutrophil granulocytes in 10 high-power fields is the best histopathological threshold to differentiate between aseptic and septic endoprosthesis loosening. In: Histopathology . 54, 2009, pp. 847-853. PMID 19635104 .
  11. ↑ L. Morawietz et al: Gene expression in endoprosthesis loosening: chitinase activity for early diagnosis? In: Journal of Orthopedic Research. 26, 2008, pp. 394-403. PMID 17902171 .
  12. ↑ L. Morawietz et al: Differential gene expression in the periprosthetic membrane: lubricin as a new possible pathogenetic factor in prosthesis loosening. In: Virchow's archive. 2003; 443, pp. 57-66. PMID 16888914 .