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261
22. Tissue Ingrowth: The Mesh–Tissue Interface
composite mesh, concluded that the bulk of tissue ingrowth happens
during the fi rst 2 weeks after implantation. At 4 weeks, the strength then
increases to a value that is equivalent to 94% of the peak strength
measured at 12 weeks postimplantation. [ 20 ]
Interestingly, not all biomaterials are incorporated into native tissue
by this cellular phenomenon equally. As early as 1995, Bellón et al.
published results that compared the cellular response to, and subsequent
tissue integration of, two different mesh prostheses in a rabbit model
[ 21 ] . At the time, products were made of only one material, either
heavyweight polypropylene or ePTFE. The authors suspected the two
materials incited different levels of in fl ammation and therefore implanted
these two meshes into the anterior abdominal wall of rabbits, ensuring
that each mesh was exposed to the peritoneal cavity. Necropsy was
performed at 14, 30, 60, and 90 days. Microscopically, the host tissue
response differed between the ePTFE and the polypropylene. At the
2-week point, the ePTFE formed a fi brous capsule without cellular
in fi ltration. Conversely, the polypropylene was integrated throughout
with loose collagen fi bers and had cellular in fi ltration consisting of
macrophages and myo fi broblasts. Collagen fi bers and neovascular
capillaries were not readily visible on the ePTFE until 2 months after
implantation. By 3 months postimplantation, the capsule tissue was
substantial, and the cell population had stabilized consisting of mostly
fi broblasts. In contrast, the polypropylene mesh demonstrated early and
complete integration into the host tissue. The process of angiogenesis
began within the fi rst 2 weeks and cells were distributed within the pores
of the mesh. They concluded that polypropylene incited a more intense
in fl ammatory foreign body reaction and that polypropylene had superior
tissue integration. Therefore, ePTFE was more suitable for implantation
intraperitoneally where it would be exposed to the viscera and that
polypropylene would be better suited for tissue integration.
The evolution of laparoscopic hernia repair pushed mesh development
to meet the unique needs of the peritoneal cavity. Two different surface
were required, one surface that optimized tissue integration at the
abdominal wall (macroporous) and another to limit visceral adhesions
and ingrowth (microporous). The fi rst of this kind paired heavyweight
polypropylene/ePTFE in a composite mesh. Ianatti et al. studied the
differences in the strength of tissue attachment to the two different
materials in a porcine model. Again, the meshes were evaluated at
different time intervals (2, 4, 6, and 12 weeks). The results showed that
the strength of tissue ingrowth was signi fi cantly higher for the
polypropylene composite graft relative to the strength of ingrowth into
262
G.J. Mancini and A.M. Alexander
the pure ePTFE material at each time point. For example, at 2, 4, and
12 weeks, the mean peel strength for the ePTFE was 0.50 pounds, 0.53
pounds, and 0.51 pounds, respectively (0.51 pounds equals 2.27 N). This
was signi fi cantly less than the peel strength of the polypropylene at 2, 4,
and 12 weeks respectively being 0.825, 1.06, and 1.12 pounds ( p < 0.05)
(equivalent to 3.68, 4.70, and 5.0 N) [ 22 ] .
The authors then looked at histology slides and found at 2 weeks,
the macroporous polypropylene component of the composite mesh was
entirely in fi ltrated with fi broblasts and in fl ammatory cells with collagen
deposition occurring throughout the polypropylene. The microporous
surface of the ePTFE, however, showed no cellular penetration through
the ePTFE at 2 weeks. There were obvious differences in the histologic
reaction and peel strengths between the different biomaterials
suggesting that tissue ingrowth and peel strength was superior for the
polypropylene layer of the polypropylene/ePTFE composite mesh
compared to a pure ePTFE material against the peritoneum. The tissue
ingrowth maturation process for the polypropylene seems to reach 74%
of its max by 2 weeks and 95% of its maximum by 4 weeks. The
strength then plateaus after a 12-week period of time in animal studies;
however, there may be evidence that cellular turnover continues for up
to a year, and the severity of the continuing process may be dependent
on the type of mesh implanted.
This degree of in fl ammation produced in response to various mesh
products was recently studied using immunohistochemical testing for
Ki-67, which is an accepted and established marker of cell proliferation
and turnover. In a rabbit study that compared tissue ingrowth analysis
between a control of polypropylene and three mesh products: a
heavyweight polypropylene/ePTFE composite mesh (hPP), pure ePTFE
(ePTFE), and a reduced weight polypropylene/oxidized regenerated
cellulose composite mesh (rPP), the authors looked at results at both 4
and 12 months postimplantation. The authors found that the hPP mesh
had signi fi cantly higher Ki-67 levels than the rPP and the ePTFE groups
at 4 months. At 12 months, a signi fi cant decrease in Ki-67 scores from
the 4-month point was found in the rPP group only, while the hPP group
maintained elevated levels of Ki-67. This interesting fi nding suggests
that the heavyweight polypropylene-based mesh material incites an
ongoing in fl ammatory process and scar remodeling that lasts even 1 year
later. This fi nding was not seen with the lightweight polypropylene
product or with the pure ePTFE. The translation of this fi nding into a
human clinical setting remains unknown but may suggest that heavyweight
polypropylene may have poor long-term biocompatibility compared to
263
22. Tissue Ingrowth: The Mesh–Tissue Interface
lightweight polypropylene and ePTFE. This poor biocompatibility may
lead to poor mesh compliance and [ 23 ] .
The compliance of the mesh implants may change over time for two
reasons. First, a thicker scar plate may form as a result of chronic
in fl ammation and collagen turnover. Second, the chronic in fl ammatory
process may cause chemical alterations to the material structure. Both
likely impact the long-term loss of mesh compliance in the mesh seen in
human explant studies. With loss of mesh compliance, the abdominal
wall becomes less pliable resulting in physical discomfort, limitations in
daily activities, and overall dissatisfaction. The group from Charlotte,
North Carolina, performed a rabbit comparison study, and within that
study, they reported on mesh compliance 1 year after implant. Using a
differentiated variable reluctance transducer (DVRT) that provided
measurements of the axial forces required to stretch the mesh, the group
reported compliance data on pure polypropylene, a composite mesh of
polypropylene and ePTFE, pure ePTFE, and a composite of lightweight
polypropylene and an oxidized cellulose layer. At 1 year, they showed
that the compliance of the pure two-sided ePTFE mesh was superior to
the other three meshes [ 24 ] .
Interestingly, using the same DVRT method to then analyze the peel
strength of the mesh products, the group did not demonstrate a signi fi cant
difference in peel strengths between those four materials, although the
heavyweight polypropylene/ePTFE composite trended toward having
the greatest peel strength. Having no signi fi cant differences in the tissue
ingrowth to ePTFE, lightweight polypropylene composite mesh, and
heavyweight polypropylene composite mesh has been shown in a number
of rabbit studies published by the same group [ 24– 26 ] . This fi nding is
not consistent with other published rabbit and porcine studies that
compared the same products [ 22, 27 ] and may be related to factors that
include the type of animal model used and the method of obtaining and
calculating the peel strength. In conclusion, while the polypropylene-
based mesh materials show superior tissue ingrowth and superior peel
strengths, the long-term loss of material compliance may result in
increased mesh failures at the mesh–tissue interface.
In a porcine adhesiogenic laparoscopic ventral hernia model, McGinty
et al. compared the 3D polyester/anti-adhesive collagen composite mesh
to the pure, two-layered ePTFE mesh (DualMesh
®
, Gore, Arizona) and
used heavyweight polypropylene as a control. After laparoscopic
insertion and survival for 4 weeks, the peel strength of the mesh from the
abdominal wall was analyzed using a digital tensiometer and found to be
signi fi cantly less for the pure ePTFE than for the polyester/anti-adhesive
264
G.J. Mancini and A.M. Alexander
collagen composite mesh or the pure polypropylene control (1.3 N/cm
vs. 2.8 N/cm, p = 0.001 vs. 2.1 N/cm, p = 0.05, respectively). Histologically,
there was excellent fi brous growth into and through the polypropylene
and the polyester component of the composite mesh. There was no tissue
growth through the ePTFE. This fi nding supports the notion that complete
tissue ingrowth can be found in a 3D polyester mesh and that this leads
to superior adherence strength when compared to the peel strength seen
with pure two-sided ePTFE [ 28 ] .
In another study, the 3D polyester/anti-adhesive collagen composite
mesh was compared to a heavyweight polypropylene/ePTFE composite
mesh (heavyweight polypropylene parietal layer) [ 29 ] . The same porcine
model was used. A pure polypropylene mesh was used as a control. While
the study reported on a number of variables, regarding the issue of tissue
ingrowth as measured by the peel strength of the mesh from the abdominal
wall, the authors concluded that the polyester composite product and the
polypropylene composite product had no signi fi cant difference in abdominal
wall adherence. This result suggests that in this study, a 3D polyester mesh
has similar fi brous ingrowth properties as the polypropylene mesh [ 29 ] .
In another prospective animal study using the same adhesiogenic
porcine model, polyester/anti-adhesive collagen composite mesh was
compared to a composite mesh made of lightweight, polydioxanone
polymer-encapsulated polypropylene on the peritoneal surface and
oxidized regenerated cellulose as the anti-adhesive barrier on the visceral
surface [ 30 ] . A regular polypropylene was inserted as a control. After
1 month, the mesh was harvested and as part of the evaluation, peak peel
strength was measured using a digital force gage tensiometer (Omega
DFG51-10 microprocessor-based digital force gage, http://www.omega.
com ). The results showed that in this study, the peel strength was
signi fi cantly higher for the 3D polyester composite mesh than for the
encapsulated lightweight polypropylene composite mesh (17.2 N vs.
10.7 N), respectively ( p < 0.002) [ 30 ] . The bottom line conclusion is that
the synthetic mesh materials are not equal, and in any given scenario,
each of the mesh materials will behave differently.
Clinical Observations and Explant Findings
The base chemical composition, the material density, and the woven
macrostructure design of a have an interrelated impact on how the mesh
will be received by the host immune system. The overall trend in mesh
265
22. Tissue Ingrowth: The Mesh–Tissue Interface
design is to create an implant that has a more physiologic biocompatibility
with the host. This means that the mesh can withstand the physiologic
stress experience by the abdominal wall and can remain minimally
altered by the host immune response over the life span of the host. The
market response to this trend has been the development of mono fi lament
materials woven into lightweight (<30 g/m
2
) mesh with wide pore spaces
[ 31, 32 ] . More data is needed to determine whether the newer lightweight
and large pore macroporous materials will deliver the desired result.
Does the Patient Matter?
To date, the primary focus on improving hernia outcomes has been
on the surgical technique. Though evolving surgical technique is crucial
to improved outcomes, the patient’s individual physiology is major
factor that must be considered. Knowing our patients unique social
habits, genetic constitution, current medical comorbidities, and past
surgical history is just the beginning of the hernia planning process.
With imperfect techniques, imperfect materials, and imperfect patients,
successful hernia surgery requires the surgeon to choose an
individualized “best- fi t” scenario. This contrasts to usual surgical
thinking that tries to de fi ne a single standard surgical technique and
apply it to all patients.
The lifestyle choices that patients make often play a signi fi cant role
in hernia occurrence or recurrence after surgery. The most detrimental
choice is that of smoking tobacco. Aside from the pulmonary function
compromise that increases perioperative morbidity and mortality,
smoking has a direct impact on wound healing and tissue remodeling.
Smokers have twice the inguinal hernia recurrence rates and four times
ventral hernia recurrence rates compare to nonsmokers. Basic science
studies show that type I and III collagen synthesis rates are negatively
affected. Also, matrix metalloproteinases, enzymes responsible for
collagen degradation, are expressed in higher levels [ 33 ] . Together, the
biologic imbalance induced by smoking shifts the wound healing toward
low-quality collagen with decreased tensile strength. In the case of a
primary hernia, the fascial integrity weakens over time. In the case of
hernia recurrence after mesh implantation, poor collagen integration may
allow failure at the tissue–mesh interface.
Genetic constitution plays a signi fi cant role in hernia development.
Rare but well-documented collagen synthesis disorders such as Marfan
and Ehlers–Danlos syndromes have high incidence of hernia. Inherited
266
G.J. Mancini and A.M. Alexander
disorders such as homocystinuria, elastosis, and congenital hip dislocation
have also shown to have an elevated incidence of hernia. Common
histologic fi ndings of all these conditions are poorly organized collagen
macrostructure. Altered cross-linking within between collagen fi bers as
well as altered ratios of type I and III collagen content is seen. Similarly,
genetic causes of poor tissue remodeling, as observed in aortic aneurysmal
disease, have increased hernia incidence. Genetic overexpression of
tissue matrix metalloproteinases leads to excessive destruction the
extracellular matrix and tissue growth factors. Altering the cell signaling
for local fi broblasts and removing critical tissue scaffolding impair
collagen synthesis and remodeling [ 34, 35 ] .
The classic predictors for poor wound healing such as malnutrition,
obesity, diabetes mellitus, corticosteroid use, immunosuppression, and
active infection effect hernia outcomes. Malnutrition and corticosteroids
suppress immune function thereby reducing collagen deposition. Obesity
generates elevated tensile forces that may overwhelm fi xation techniques
at the tissue–host interface and is associated with increased surgical site
infections. Diabetes impairs macrophage function and fi broblast
migration and alters the balance between the accumulation of ECM
components and their remodeling by MMPs [ 36 ] .
Summary
Mesh implants require suf fi cient integration within the host tissue to
prevent dislocation and reduce recurrences, and knowledge regarding
tissue ingrowth at the mesh–tissue interface is still evolving. Successful
outcomes from a hernia operation are dependent on optimizing for each
individual patient the choice of the surgical technique and the implant
materials. We know that the prosthetic materials we implant in patients
during a hernia repair are not inert to the body’s immune response and,
on the contrary, are likely to dictate the fi nal strength of the MTI ingrowth.
The base material composition and three-dimensional macrostructure of
the mesh impact the body’s response. We know that an individual’s
immune response to the implant is highly variable and poorly understood,
and genetic variance in the immune response may have a signi fi cant role
in modulating the foreign body response. We know that mesh materials
are implanted in a wide variety of locations in the body and applied with
different surgical techniques. Further human basic science and clinical
research is needed in this area.
267
22. Tissue Ingrowth: The Mesh–Tissue Interface
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B.P. Jacob and B. Ramshaw (eds.), The SAGES Manual of Hernia Repair,
DOI 10.1007/978-1-4614-4824-2_23,
© Springer Science+Business Media New York 2013
23. Patient Comorbidities Complicating
a Hernia Repair: The Preoperative
Workup and Postoperative Planning
Scott Philipp
Abdominal wall hernias are a common problem encountered by
medical practitioners. Their contribution to chronic pain and loss of form
and function are reasons why they often come to the attention of the
hernia surgeon. Hernia surgery continues to evolve at a frantic pace, with
many differing techniques and products available, and better results
being reported. However, complications from hernia surgery still abound
and recurrence rates, especially in certain patient populations, leave the
surgical community looking for better answers. As we continue to learn
and improve, several comorbid conditions need to be considered prior to
embarking on the surgical treatment of an abdominal wall hernia.
Recognizing the presence of these potentially complicating factors and
optimizing them prior to surgery will ideally increase the success of the
surgery and the positive impact on the patient’s quality of life.
Comorbid Conditions and Considerations
Surgical History
It is of primary importance to elicit a complete history of any previous
abdominal surgery prior to proceeding with repair of an abdominal wall
hernia. If previous operations were performed at outside institutions, then
efforts should be made to obtain those operative reports to assist in
preoperative planning. The presence of intra-abdominal scar tissue cannot
be evaluated preoperatively although it should always be considered and