Biomet Cementing University

Pathogeneses

Periprosthetic infection must be clearly differentiated from other bone infections, such as osteomyelitis, as a foreign body is involved. The host recognises as enemies not only bacteria but also foreign bodies, both of which are handled in the same manner by the human body. And both micro-organisms as well as foreign materials induce inflammation as a reaction to tissue injury.

As the first line of defence, macrophages try to degrade these materials by enzymatic digestion. But if the foreign body is too large for the macrophage, fibroblasts are stimulated to form granulation tissue and giant cells around the foreign body, inducing, as with tuberculosis, a specific morphological lesion: the foreign body granuloma. Finally, the foreign body is encapsulated by a tight, dense membrane of connective tissue.

In artificial joint replacement, slight interfacial motion is associated with resorption and remodelling of the bone bed, activation of macrophages and production of wear particles, followed by formation of an interfacial membrane. Gristina described this process as resulting in an immune-incompetent fibro-inflammatory zone surrounding biomaterial implants.

Like the fibroblasts, many bacteria, especially staphylococci, are able to colonise the surface of the foreign body. The race of the fibroblasts, activated by the macrophages, against the bacteria to colonise the foreign body is called by Gristina “the race for the surface“.

Brisou has stated that the process during which bacteria become bonded to foreign surfaces is divided into three steps:

Adsorption mediated by the physical chemical properties of the surface
Adhesion a specific mechanism of stereochemical molecular recognition
Adherence the state in which bacteria are anchored to the surface by forming biofilm

The first two steps, adsorption and adhesion, are completely reversible. Adherence, on the other hand, is irreversible because of the biofilm it involves.

Biofilm is a slime in which germs can live comfortably because the slime protects the germs from dehydration and attacks the host defence. When bacteria colonise inorganic surfaces, they change character. Adherence by biofilm severely reduces the susceptibility of bacteria to antibiotics, as the bacteria living in biofilm are more resistant to antimicrobial agents owing to a prolonged doubling time (of up to 20 hours) and a slow turnover. Additionally, the extracellular slime itself is able to inhibit the antimicrobial action of glycopeptide antibiotics.

Although colonisation and slime formation alone do not cause an infection or an infectious disease, bacteria can spread along the surface of an implant very slowly, and signs of infection may occur later, when the bacteria leave the site of the interface, invade surrounding tissue and induce secondary osteomyelitis. In fact, our experience relates that only 50% of deep infections of artificial joint replacements occurring within a post-operative period of ten years become manifest during the first year after implantation.

Most pathogens, such as coagulase negative staphylococci or propionibacteria, are regarded as low grade and unharmful to patients. But in the event of periprosthetic infection, some pathogens can lead to life-threatening septicaemia. Staphylococcus epidermis and staphylococcus aureus are the germs most frequently isolated from biomaterial surfaces. Other micro-organisms, including propionibacteria, streptococci, corynebacteria and pseudomonas, may also cause infection.

Bacterial pathogens theoretically are able to reach the prosthetic device in any one of three ways:

By direct contamination during the surgical procedure (from the patient's or surgeon's flora or from contaminated air in the operating room)
By way of the bloodstream (in the case of bacteriaemia or septicaemia)
By continuous spreading from an adjacent infection (induced by erysipelas, for example)

Lidwell has stated that over 95% of periprosthetic infections occurring during the first year after artificial joint replacement are due to intraoperative contamination of the prosthesis. A haematogenous origin of infection is typically associated with infections occurring later. In this case, the pathogen is transported from a distant site of infection (for example from an infection of the teeth or the bladder) by either the bloodstream or lymphatic vessels to the prosthesis.

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