Pleats and creases that form naturally in shell severely limit product durability. The problem is worse for implant styles that incorporate design features that facilitate pleating. Others have semi-rigid features which create high stress pleats in vulnerable areas. Patches, filling ports and fixation appendages are strong factors in the formation of destructive pleats and puckers which concentrate fatigue and focally strain the material beyond its elastic limits.

These features can greatly increase the risks of rupture and magnify injuries by insidiously releasing progressively larger quantities of the filling substances with time thus dulling the user’s perception of problems . Intracapsular spaces gradually flood with oils and gel by-products and users do not perceive the changes in sensation dramatically. They are thus motivated to delay action until the problems become severe as the oil/gel infiltrated tissue masses become palpable or when systemic problems develop.

Many shells consists of incorrectly formulated and poorly processed elastomer parts. Usually, the crosslink density is insufficient or non-uniform. Such shells are subject to plasticization primarily from low molecular reactive oils and degradation products released by the gel. The mixing of gel with aqueous substances in the presence of catalytic impurities leads to loss of crosslinks and reduction of molecular weight in certain formulations. Low molecular weight entities formed in most instances.

The shells of used implants are frequently found swollen and distended. Typically, about 10 % linear swelling is encounted. The phenomenon is visible on simple inspection. Patches and injection port boundaries, in particular for implant designs incorporating fabric reinforcement, show stress pleats radiating peripherally. This confirms significant changes in surface area of the shell as a result of physico-chemical alterations of the material as low molecular products interact with the elastomer.

As shells expand, surface area is created and the devices become somewhat underfilled. Pleating, involution and invagination of the shell takes place with greater ease. Low profile items are specifically prone to the problem and their performance is much worse than the more puffy high profile versions which have less excess surface area.

Shell shows pleat patterns which are specific to shell styles and to the degree of filling. Severe pleating culminating in loss of shell integrity is encountered in most implants after about 7-10 years in vivo. Such pleats may have been less prominent shortly after implantation as the shell may have been less swollen and thus would have behaved as if I was more fully filled. surplus surface area.

Certain designs incorporating aqueous media are notorious for releasing these fluids over time. Saline inflatable implants, mixed gel-saline devices and multi-lumen prosthese gradually leak their aqueous additives. As a result, they lose part of their volume and become grossly underfilled. Pleating becomes more severe and crease line fatigue rapidly lead to small shell perforations; eventually the perforations enlarge to become gross rupture sites which progress with time and movement.

Failures of this kind are typical of silicone elastomer shells manufactured according to processes which prevailed throughout the industry from the seventies to the nineties. Items manufactured in the early-eighties were particularly affected by the process. They account for more than 60 % failure rates in all such series.

For example, the mixed gel-salines of the "Wood" type have anextemely poor record of durability and most show severe pleat and fatigue-induced ruptures with significant losses of gel/oil. This is the result of changes in the shell ultrastructure aided by focal degradation of the elastomeric material at points of stress concentration. Cyclic folding and rolling or displacement of the pleat line associated with normal in vivo usage is a dominant factor in accelerating the process. Contracture of periprosthetic capsules contribute significantly to early ruptures as it increases compression on pleats. In most cases, the process rapidly leads to visible crazing at pleat sites, especially areas which show confluency points and cross-over of pleats and pucker zones.

Stress concentration in polymers increases the reactivity of such materials at the stress sites. This is observable for all thermoplastics. Elastomers, in particular plasticized elastomers with high levels of impurity and irregular crosslinking introduced through secondary reactions (vulcanization), are also suject to the effect. Failures of this kind dominate breast implant studies.

For explanted prostheses, the average pleat failure antedate the surgical removal by many years as evidenced by the extensive development of deep pleats with drastic focal changes in elastomer properties.. Crazing on pleats and refractive index changes are universally encountered for thick-shelled implants. Once crazed, the affected areas rapidly become porous allowing further leakage of low viscosity substances. There is concurrently a reduction in mechanical properties of the shell. This impacts adversely on tear strength, elongation and tenacity.

Approximately 1-3 years of supplemental dwell time are generally needed for development of grossly visible shell rupture points. Progression of fatigue-induced damage takes place at a rate which is related to the user's level of activity and is affected by the relationship of the devices to the chest structure and the user's work habits. For underfilled or swollen implants, compression is not a significant factor in the enlargement of perforations. Contrary to frequently expressed opinions from individuals not fluent with elastomeric material properties, such shell failures show unique characteristics. They are unrelated to trauma, impact or surgical mishandling. It terminal stages, the condition of the shells becomes so unstable that they cannot even sustain movement and stresses of explantation surgery without further propagation of failure lines.

The processes of pleat-induced rupture and shell fatigue failure have been well known in select circles of plastic surgery insiders and within the breast implant industry. Complaints, litigation, product returns and business records spanning more than 25 years address these issues.

Users of mammary prostheses are subject to special modes of injury which result from the presence of a foreign object placed below a thin skin cover; this object acts as an ‘anvil’ by concentrating the force of a traumatic event against the overlying tissue. The possibility of damage to an impaired prosthesis from trauma also exists but is overshadowed by what occurs to surrounding tissue. With widespread use of compression capsulotomy as a ‘therapy’ for contracture, iatrogenically-induced trauma is also a major user risk.

It is normal to expect injuries from traumatic events. It is also logical to expect the magnitude of the injuries to reflect the severity of trauma. Subjects with prosthetic systems in the upper chest area are not exempted from these rules. However, the mechanism of injury and the type of injury differ substantially from normal subjects. In addition, prosthetic damage which may result from the trauma is not what is expected on the basis of simple anatomic considerations. The intercalation of a large, soft and elastic device within a comparatively large mass of soft tissue drastically alters the biomechanical properties of the area and modifies the behavior of the mass to the point where new types of injuries must be considered.

Primary impact and crushing injuries to the upper chest area include mostly hard tissue damage, rupture of blood vessels leading to hematomas and seromas, glandular tissue injury leading to oedema, nerve damage culminating in late pain, cartilage trauma, and separation of muscle attachment points, muscle damage associated with overextension and deep trauma involving transmission of energy to more fragile internal organs, such as the liver. In many patients, this translates most frequently as rib cage injury such as fractures with associated secondary soft tissue damage. These are commonly encountered under trauma conditions and are generally expected by clinicians who habitually treat accident victims. For subjects with prostheses, all of the above damages are possible.

Other types of injuries are often encountered. Frank damages to sound prostheses are encountered but are comparatively rare. Failed prostheses or severely aged devices which are already compromised can lose their integrity and release their content. Simultaneously, the tissue pocket (prosthetic capsule) is often ruptured. As a result, gross contamination of surrounding tissue by prosthetic debris is amongst the secondary sequelae. Such material can spread and extrude deeply within muscle planes and may reach well beyond the confines of the original prosthetic site. Extrusion to the axillae and the upper arm are reported as well as downward extravasation into the abdominal area. Curiously, prosthetic damage can be demonstrated to have pre-existed the traumatic events for most cases studied to date.

The presence of prostheses in a traumatized area magnifies injuries and complicates the emergency treatment. They may also create conditions where emergency care is not sufficient. Instead, policies advising a more prolonged follow up to forestall late complications and ensure appropriate clinical management of late sequelae may be necessary. The most frequent complication results from bleeding within the prosthetic space. Other complications include post-traumatic infections from release of accumulated micro-organisms within the prosthetic space (intracapsular colonization). Failure or avulsion of valves parts on saline-filled prosthetic systems can account for other post-trauma complications with late sequelae.

Failure of the prosthetic device is not a dominant preoccupation for comparatively new implants. Devices with less than 4-5 years of dwell time and of reasonable quality do not fail from traumatic events, least of all impact. Perforation damages are possible but these are rare. Yet there are numerous anecdotes claiming rupture of implants from trauma. The episodes appear largely inaccurate on detailed analysis. Implants claimed to have suffered failure as a result of trauma were, in all cases studied by this facility, either already ruptured and partly contained within the tissue capsule or else the shells were severely compromised through pleating, fatigue, abrasion or material deterioration.

Implants, when new, are surprisingly hardy or "elastic". They remain that way for a certain period of time, usually about 4-5 years. Studies performed by Dow Corning in connection with the defense of product liability claims support this view. Dow Corning experts further claim (Turner v. Dow, Colorado, 1993) that prosthetic devices can sustain enormous pressures that far exceed any realistic impact or sustained compressive trauma. They further claim that the devices remain that way indefinitely. According to the Dow Corning defense position, there is no basis to fear failure of prostheses from pressures that may be generated by a vehicle accident or deliberately induced "therapeutic compression capsulotomy" that would not cause gross anatomic damage such as broken ribs.

Such a position has validity only in the first few years of dwell time for some types of new prostheses. Shortly after implantation, the properties of the shell begin to change and eventually after 5-10 years shell failure takes place even without significant externally-induced trauma. This is a material problem and is the result of aging, "coldworking" and fatigue along pleat lines. Aging and deterioration occur through chemical, physico-chemical and mechano-physical processes. The decisive factors arise from repetitious movements associated with daily occupations. Concurrently, the implant shell materials decay by loss of bonding between the filler particles (silica reinforcement additives).

Penetration of the shell elastomer by interactive biological substances such as lipids adds additional factors which lead to losses in mechanical properties; these are termed "plasticization phenomena" and frequently lead to major losses in mechanical properties. The problem was encountered first in the sixties in connection with cardiac valve components. Outright chemical changes can also take place in some classes of formulated silicone elastomers; these affect parts of the siloxane backbone and/or the crosslink sites which incorporate residual (impurity) unsaturation (double bonds) and other reactive chemical groupings that are induced through side reactions.

Parasitic or side reactions introduce such defects in the molecular network of elastomers thus enhancing their chemical vulnerability. The formation of vulnerable segments in the elastomer network takes place concurrently with normal synthesis (polymerization) of the primary polymer components and during the crosslinking reactions that lead to the finished elastomers. These anomalous chemical sites can occur in large numbers under coarse industrial preparative conditions.

Mechanical phenomena superpose on chemical deterioration. Mechanical properties of the elastomers are severely changed along crease lines and in areas subject to repetitious flexing and bending. This kind of deformation is almost universally encountered in explanted breast prostheses. These items suffer the predictable result of having been haphazardly packed into a prosthetic space for a long period of time. Specific geometric patterns of pleating that vary according to the prosthesis type, size and position are noted. The deployment of such devices within the breast pocket is particularly critical in that respect; contracted capsules around severely pleated implants tend to induce early failure.

Calcified capsules are precursor signs of early failure along pleat lines through abrasive phenomena. Calcific entities tend to excoriate the shell at prominent pleat points; this is particularly notable for devices which form large organized crystalline aggregates in the intracapsular space (margin calcification). Devices surrounded by such debris inevitably culminate in shell failure by mixed abrasive and fatigue-inducing processes. They may not be grossly ruptured as long as the periprosthetic capsule is in place undisturbed. However, minor trauma including that from daily occupations, is sufficient to complete the damage to full ruptures in many instances. At any rate, rupture ultimately develops even without trauma.

After approximately 4-7 years, implants develop a significant number of flaws and most have severely compromised shells. The more durable kinds tend to be the ones manufactured from simple shell configurations which are fully filled. This type of structure does not pleat as easily and assuming that gross chemical deterioration of the shell material has not taken place, perforations occur late. Most, however, though not grossly perforated or frankly ruptured show microscopic damage zones which coincide with planes of weakening. These clusters of defects are mechanically equivalent to the "dotted perforations" found on paper documents that have detachable portions where machine-made perforations facilitate precise tearing along dotted lines.

Trauma associated with vehicle accidents and falls are of less importance than deterioration or slow compressive trauma. This has to do with the nature of the gel. Silicone-based filling gels that are correctly engineered have marked viscoelastic properties. At high rates of deformation such as may be met during a severe impact, they behave nearly as "solid" objects; they do not deform substantially on impact. Instead, they transmit energy to the support structures, usually the rib cage. The result is rib fracture and tissue damage to the chest. Capsule damage then subsequently follows, usually resulting in a rupture involving the upper medial anterior zone, an area where the tissue wall is generally the thinnest. Within the next few seconds, deformation of the shell does indeed take place and may complete the apparent failure of an already ruptured or compromised shell with severe extrusion of the gel. However, for a sound shell, the impact will leave the prosthesis undamaged and only tissue damage is observed.

Slow compression with a very large deformation can occur in a collision where the occupant is compressed and immobilized for a substantial period of time within the crushed vehicle space. An equivalent situation would be met by someone constrained within an array of seatbelts for several minutes. These situations may cause sufficient deformation to rupture an already compromised implant. However, unless the applied pressure causes enormous deformation such as total flattening of a prosthesis to a thickness of less than 1 cm, rupture will not take place. Instead, a rupture of the surrounding tissue may result.

Deliberate application of compression to the breast is used for mitigation of contracture. It is termed "closed capsulotomy" or "compression capsulotomy" and was at one time habitually prescribed for implant users with capsular contracture, a condition that may affect as many as two patients out of three after five years of dwell time. According to certain physicians, this traumatic rupture of the capsule through compression was thought to be a "beneficial result".

In summary, vehicle accidents or other traumatic events which cause impact to the upper chest do not habitually result in prosthesis damage. Instead, the periprosthetic tissue and structures may be more damaged than expected and the damage may be subtly different from what is normally found in normal accident victims. In addition, the presence of the prosthesis can hide more serious damage or delay the onset of key diagnostic symptoms. Hidden or delayed injuries include subtle rib fractures, the formation of intracapsular hematomas, muscle and cartilage detachment from the skeletal structure, rupture of blood vessels, impact damage transmitted to the more fragile internal organs (liver trauma) and other tissue damages that can be induced through large scale deformation. Adhesions between the capsule tissue, the breast structure and the chest muscles can often add other dimensions to such injuries. However, events that do not lead to severe and prolonged compression or penetrating chest injury rarely have permanent damaging effects on the prostheses.

The type of vehicle or event-induced trauma is also a key factor. Prosthetic damage can be expected for old devices, in particular if there is a large and sustained deformation such as may be expected when an accident leads to a vehicle compartment that is drastically crushed. Such a situation habitually leads to prolonged compression of the chest between the instrument panel or the steering assembly and the vehicle seat. A prosthetic rupture however requires enormous crushing loads maintained for significant periods of time, in effect a situation where the occupant is trapped in the vehicle. Elastomers of the type used for breast prostheses have the ability to sustain large deformations when correctly manufactured. These deformations can be more than five to tenfold the original linear dimension of the material. For an average prosthesis, this means that the diameter of the device can be expanded by at least three to four times by compressing it. This is rarely possible without massive concurrent anatomic injury. Perforating trauma can occur from protruding objects which break the skin. These events can lead to frank tears or "shell rupture" through a combination of perforation, cutting, tear initiation and tear propagation but these are rare and are more typical of "anti-personnel" or "assault and battery" trauma.

Damages are frequently created when prostheses are removed. Such damages can affect surrounding breast tissue as well as the prostheses. Ruptures can result from accidents surrounding the procedures such as instrument strikes and inaccurate cuts. Typically, scalpels, hypodermic syringe needles, Metzabaum scissors, bone rongeurs and other cutting devices can inflict damages to the prosthetic system. In some cases, the damages can have long term health implications for the users.

Surprisingly, electrosurgical instruments such as Bovie units do not cause specific prosthetic damage on their own. The insulating nature of the prostheses and much of the debris precludes cutting action and thus the devices are ineffective in non-conductive, non-tissue areas. Similarly, certain procedures surrounding explantation which appear a priori destructive may be comparatively benign. Examples include pericapsular dissection which may involve compression of the integrated capsule-implant composite. Blunt pericapsular dissection is also relatively undamaging to a mechanically-sound prosthesis. Devices already ruptured or compromised through fatigue action, multiple fatigue and erosion-induced perforations can nevertheless suffer exacerbation of the damage from the procedures.

Other situations can also occur and, to the eye of the surgeon or the pathologist, the devices may appear superficially "intact" or "unchanged" at the outset and then appear to undergo ‘rupture’ during the surgery . Detailed examination of many records from explantation procedures frequently reveals notations indicating the surgeon believed rupture took place sometime during the removal procedure. Other records indicate that "intact" implants were removed but that the devices were subsequently found to have "disintegrated" upon standing or in the container. Such situations are not consistent with findings from subsequent detailed examination of the explanted material. Sound implants with brief dwell times in vivo do not disintegrate during explantation surgery. Conversely, failed devices with major rupture sites can mimic "intact" implants and appear superficially unchanged to the eye of a surgeon not wholly knowledgeable in the configuration, construction and fabrication techniques of breast implants.

One of the most frequent misconceptions is associated with the removal of multi-lumen implants and with implants incorporating fixation systems. Multi-lumen implants have very brief service lives and are generally explanted with ruptured outer shells. Frequently, the rupture sites, even when large, are imperceptible except on very detailed examination as the outer shell is collapsed and retained very close to the inner shell by a layer of extravasated oil/gel. The appearance of an "intact" implant is therefore very convincing in spite of frequent rupture perforations and gross extravasation of these devices. Furthermore, determining whether or not such implants are ruptured requires prior knowledge that they were double lumen configurations to start with.

Some types of double lumen implants have totally independent inner shell core assemblies. The outer shell is in turn very similar to saline implants of the seventies. Ruptures involving such devices can lead to even more confusing situations to a surgeon and even to a specialist in implant design. Many manufacturers produced multi-lumen implants using standard gel-filled prostheses for the core. Rupture of the outer shell occasionally leads to frank separation of this part and its discrete re-encapsulation in a separate prosthetic pocket followed by the re-encapsulation of the "intact" gel-filled core into a superficially normal secondary capsule. Such a situation has caused some users to have only the gel-filled core removed whereas the outer shell was left in a remote part of a separately formed secondary capsule. Subsequent routine radiological studies for recurring complaints occasionally uncover shell fragments, valve parts or extravasated material from failed prostheses which were noted in surgical reports to have been explanted "intact". To further confuse the situation, the attempted identification of the core of such implants by individuals not knowledgeable on assembly and identification techniques leads to an incorrect identification where the core part is identified incorrectly as an automous gel-filled implant.

Other situations involve anecdotes from surgeons reporting the removal of "intact" implants which contain a multiplicity of small perforations coincident with invaginated parts of the shells. Such damages frequently remain unnoticed until the prostheses are examined or handled at which time they appear to "disintegrate" or "fall apart" in the hand of the observer.

The opposite situation also exists. Explantation records contain references to prosthetic pockets filled with only gel showing no evidence of shell parts. These are sometimes referenced as "disappearing shells" and such reports can be found in product returns to manufacturers and distributors. This type of occurrence is also impossible. Even the most improperly designed and fabricated implants will still leave recognizable fragments of shell. It may be necessary to sieve the degraded filling material to recover the parts or else perform some other separation but components will be found and they will reveal the causes of the failure.

Considering the manufacturing technologies used to make implants, the inadequate materials and the poor assembly practices used to make breast implants, it is inevitable that a very large fraction of items released to commerce will undergo severe mechanical, physico-chemical and molecular changes with dwell time in vivo. As these changes take place, there will be potential for major adverse health impact through classical physiologic and toxicologic mechanisms.

Older series of implants incorporating fixation systems are noteworthy for ruptures on the equator, in particular at the upper quadrant for ovoid type prostheses. Such ruptures take place nearly in coincidence with clustered pleats that form at the equator usually at points of peak curvature such as the upper and lower quadrant. The apex is also vulnerable for some types of prostheses; it is an area of stress concentration and sharp curvature. Implants fitted with stiff fabric overlays and shell patches of much greater thickness than the shell material have other problems related to the stress concentration that takes place where there is an abrupt change in the flexibility of the devices such as at edges of these overlay structures.

Clusters of fabric fixation patches of the type that were used mainly by Dow Corning in the sixties and seventies, are outstanding examples of adverse effects of these stiff appendages on the durability of the shell. Even the thick shelled "Cronin" type implants have a propensity for failing at the fixation patch edges and at the seam between the anterior and the posterior side. All of these areas are well suited for hidden failures which are not revealed until the devices are removed and are allowed to deconvolute and ‘relax’ on flat surfaces prior to examination. Even then, with gel extravasation, gross ruptures can still remain hidden.

Fabric fixation patches such as used by Dow Corning and perforated plastic fixation plates typical of Heyer Schulte and McGhan also have the propensity to initiate early ruptures and can mask such damages. They can also leave a surgeon with the impression that the rupture was the result of the explantation. Such fixation appendages are often embedded deeply into the chest wall and effectively lock the items in highly stressed conditions. Over time, the boundary between the fixed patches and the adjacent shell evidently fatigued and precipitates the disintegration of the shell material at that site. The processes are exacerbated by abrasive action from the calcified plaques which surround fixation type implants. In nearly all instances, features of the failure site are consistent with natural time-dependent damage. Some show exacerbation of the rupture line which presumably took place during surgery and/or storage.

For Dow Corning "Cronin Technique" implants, the equator and the patch boundaries are markedly vulnerable to fatigue-induced pleat failure. Natural movement associated with the user's daily occupations causes the material to undergo fatigue; body fluid penetrates the elastomer and in combination with the alkaline environment created by the calcifying tissue, the physico-chemical deterioration rapidly accelerates until there is gross disintegration of the material. Long dwell time leads to progressive damage which has specific morphological characteristics unlike the damage that is created by tearing action or other stressed mechanical situations. Natural wear-related damage is distinctive from trauma type damage. Typically, changes in refractive indices, unique light scattering phenomena and fine comminution of the shell material are precursors to frank shell failure. Deteriorated areas in prostheses with long dwell times have nearly no residual mechanical strength. They are discontinuities in the shell where only a few fragments of elastomeric material retain the shell edges together.

Defects of this kind leak mobile fractions of the filling fluid and allow natural body fluids to enter the shell, frequently leaving large pools of debris dispersed within the gel. The shells are clearly 'ruptured' but because of the comparatively stiff consistency of the filling material, the portions of the shell remain loosely held together. The capsule space is nevertheless flooded with effluents from the filling material and the shell surface is coated with the degraded substances which have egressed from the core. These are normal and expected situations for prostheses of this kind.

During explantation surgery, a surgeon faces a difficult situation. Firstly, the breast is unnaturally stiff because of the presence of the non-compliant prosthesis, the severely fibrosed peripheral tissue and the deep mineralization. Wit fixation type implants, the posterior side of the device is bonded against the chest wall and there is no easy means to access this area without stressing the surrounding structures.

Freeing the fixation patches from the chest muscle requires elaborate extracapsular dissection . The patches themselves cannot be normally separated to free the implant from the tissue-patch composite; the complete assembly must be left in situ during the dissection. At that point, the already ruptured prosthesis begins to show its rupture sites. As the dissection progresses, the rupture of the device becomes more obvious and a surgeon not knowledgeable about the construction and the behaviour of such implants is left with the impression that the item was damaged during the removal or that it "ruptured on removal". This is not so. The shell did not have integrity to start with. Ruptures of this kind normally antedate the removal by many years. In some instances, their failure is evident on radiographic studies.

Exacerbation of existing ruptures is possible during surgery by less skilled surgeons but is comparatively rare. Shell material that has not been subjected to repeated cyclic movement remains comparatively strong for many years and is usually resistant to propagative tearing incidental to explantation surgery.

Mechanically-induced shell damages, whether they occur by compressive trauma, mammographic studies or during explantation, are easily differentiated from that which occurs through natural time-dependent phenomena. Fatigue in particular is easily recognized as it takes place close to shell portions which have suffered grossly visible changes in material characteristics. Surgical instruments leave even more distinctive marks. Implants surrounded by calcified capsules erode concurrently and show a wide range of unique phenomena which cannot be duplicated by any artificial process. Instances of gross focal erosion with more than 50 % of the shell thickness abraded away are commonly found when the implants surrounded by highly organized calcified capsules. This is almost universally found in users of "Cronin Technique" and "Williams" style implants of the sixties and early-seventies.

Prostheses and prosthetic appendages eroded from chronic abrasive action by the calcified tissue show characteristic wear patterns which often superpose on fatigue damage and grossly visible pleats. This type of damage, however, is particularly distinctive and is almost always found on "Cronin" style devices. Pleats and fatigue lines are also generally present at the equator, in particular for the older style of implants which have a palpable seam between the anterior and posterior side. Fixation patch edges are vulnerable to fatigue, erosion and stress concentration. Ruptures and failure lines made up of colinear perforations are generally coincident with disturbed, eroded or pleated shell zones. Thus, the failures are unrelated to the removal surgery. The semi-solid filling substances which often still occupy the core position and show a shape memory, can maintain the outward shape of the implants. This is frequently what a surgeon first sees when the capsule space is reached. Thus, an impression is created that the device is "intact". Upon attempting to dissect the thick mineralized capsule from the chest wall, it then becomes obvious that the device is ruptured. However, many surgeons interpret the observation as being consistent with a ‘rupture at removal’.

Breast implants and related products habitually undergo deep changes. They also initiate changes in the surrounding tissue, sometimes by absorbing and converting natural biological substances from the host into modified products with adverse health implications to the user. This process takes place in the intracapsular space and within folds of the shell which entrap tissue and proteinaceous fluids.