Skip to main content
main-content

Tipp

Weitere Artikel dieser Ausgabe durch Wischen aufrufen

06.08.2018 | review | Ausgabe 3-4/2019 Open Access

Wiener Medizinische Wochenschrift 3-4/2019

Bladder augmentation in children: current problems and experimental strategies for reconstruction

Zeitschrift:
Wiener Medizinische Wochenschrift > Ausgabe 3-4/2019
Autoren:
Sophie Langer, Christine Radtke, Eva Györi, Alexander Springer, Martin L. Metzelder
Abbreviations
CIC
Clean intermittent self-catheterization
MRI
Magnetic resonance imaging
SIS
Small intestinal submucosa

Introduction

Loss or malfunction of the lower urinary tract may cause urinary incontinence and chronic renal failure. The most common underlying conditions are spinal dysraphism (spina bifida), congenital malformations (exstrophy-epispadias complex, cloacal malformations) and trauma. Modern treatment of lower urinary tract dysfunctions consists of clean intermittent catheterization (as proposed by Lapides in 1972 [ 1]), medical treatment (anticholinergic medication and botulinum toxin A [ 2, 3]) and surgical reconstruction (augmentation cystoplasty, creation of a catheterizable conduit [ 4, 5]).
In this article we review various conditions and surgical options, and highlight new concepts for the use of biomaterials and tissue engineering in the field of urinary bladder reconstruction.

Clinical presentation and issues

Neuropathic bladder

Neural tube defects represent one of the most common birth defects (33–52/100,000 live births [ 6, 7]) as well as the most common cause of neurogenic bladder dysfunction [ 8]. In this regard, there is high accuracy and precision for obtaining the diagnosis by antenatal ultrasound [ 9].
Clinical presentation of neuropathic bladder includes incontinence, recurrent urinary tract infection and, if left untreated, chronic renal failure and end-stage renal disease [ 10]. Bladder dysfunction is caused by detrusor and/or sphincter over- and underactivity (detrusor sphincter dyssynergy). A high-pressure and low-compliance bladder causes destruction of the bladder architecture, leading to diverticulation and loss of contractility, subsequently to vesicoureteral reflux, chronic renal failure and incontinence [ 10, 11].

Congenital malformations

Several rare anatomic malformations of the urogenital tract can cause bladder dysfunction as well, and are often diagnosed via prenatal ultrasound or magnetic resonance imaging (MRI) [ 12, 13]. Urogenital malformations that might require bladder augmentation include cloacal exstrophy (~0.19/100,000 live births [ 14, 15]) and bladder exstrophy (~3.3/100,000 live births [ 12]). In both entities, the volume of the urinary bladder is compromised, as is the compliance of the bladder wall. Again, insufficient treatment can lead to renal impairment [ 13].

Therapeutic options

Modern treatment of lower urinary tract dysfunctions consists of
  • Clean intermittent catheterization (CIC)
  • Medical treatment (anticholinergic medication and botulinum toxin A)
  • Surgical reconstruction

Clean intermittent catheterization

Clean intermittent self-catheterization (CIC) was introduced in 1972 and revolutionized the treatment of bladder dysfunction [ 1, 16]. CIC effectively lowers the intravesical pressure, provides urinary continence and consequently acts as protection against renal failure. It is the baseline treatment of bladder dysfunction and is also used in children with malformations of the exstrophy complex in addition to surgical management [ 17].

Pharmacological non-surgical treatment

Anticholinergic oral medication (i. e. oxybutynin) and muscle relaxation drugs in combination with intermittent self-catheterization poses an excellent option for long-term treatment in cases with neurogenic bladder dysfunction [ 1820]. Side effects of the medical treatment include anticholinergic symptoms like drowsiness, flushes and palpitations. Additionally, a high compliance is needed, but in 75–90% [ 2, 20] of all patients with neurogenic bladder dysfunction, this non-surgical treatment shows good results. In case of persistent high intravesical pressure, submucosal injection of botulinum toxin A is implemented [ 21, 22].

Surgical treatment

Bladder augmentation
If medical treatment and/or interventional methods have failed, and high intravesical pressure and urinary incontinence or recurring urinary tract infections persist combined with present vesicoureteral reflux and impaired renal function, surgical treatment in terms of bladder augmentation is indicated [ 8, 23]. Urinary bladder augmentation-reconstruction includes and simplifies:
  • Augmentation of the bladder capacity
    • via enterocystoplasty
    • or autoaugmentation
  • treatment of incontinence
  • catheterizable conduit (Mitrofanoff appendicovesicostomy)
The median age of children with neurogenic bladder dysfunction who undergo bladder augmentation is 12 years and more than half of these patients have spina bifida as the underlying disease [ 5]. In anatomical malformations, bladder augmentation is considered earlier than in children with neurogenic bladder dysfunction; the median age of those children is 6.4 years [ 15, 24]. The success rate of bladder augmentation with regard to the increase in bladder capacity as well as reduced intravesical pressure is high. In addition, the progression or the occurrence of kidney dysfunction can be avoided. Nonetheless, bladder augmentation requires close monitoring and further treatment of incontinence, and, thus, creation of a catheterizable Mitrofanoff conduit by use of the appendix vermiformis or small bowel is often part of the augmentation procedure [ 13]. In this regard, a catherizable urinary stoma may be crucial in the upkeep of the patient’s compliance to prevent short- and long-term complications such as mucous plugging and chronic renal disease [ 25].
Ileum is most commonly used to perform an augmentation cystoplasty (Fig.  1), followed by colon and stomach [ 5, 15]. Complications include small bowel obstruction, haematuria-dysuria syndrome, and an increase of urothelial cell carcinoma [ 5, 26]. In rare cases, the ureter can also be used for cystoplasty. However, ureteral dilatation with ipsilateral impaired renal function with no vesicoureteral reflux are prerequisites [ 5]. In even less cases, autoaugmentation (vesicomyectomy or vesicomyotomy) can be performed, but only in patients with a preoperative bladder volume of 75–80% compared to normal sized bladders of healthy individuals. Fibrosis and regrowth of the detrusor muscle with need for surgical revision have been described [ 5].
Although the incidence of short-and long-term complications is high, patients report a significant improvement in their quality of life [ 13].
Current risk factors and morbidity
Current risk factors and morbidity associated with bladder augmentation by non-urothelial tissue are shown in Table  1.
Table 1
Complication profile in bladder augmentation using gastrointestinal tissue
Complication
Incidence (%)
Bowel obstruction
3.2–10.3
Bladder calculi
15–40
Bladder perforation
2–8.6
Excessive mucous production
−100
Metabolic acidosis, metabolic deterioration
−100
Malignant transformation of bowel/tumour formation
0.5–10
Exposing non-urothelial tissue to urine causes a complex of problems. Through the constant contact of intestinal mucosa with urine, the accumulation of nitrosamines and infections can lead to premalignant and malignant degeneration in the long-term with incidences of 1.2–10.3% [ 5, 2733]. In a recent review, Husmann et al. suggested that the primary bladder dysfunction as opposed to the augmentation cystoplasty is responsible for the development of intravesical neoplasia [ 25]. Moreover, bladder calculi with 15–40% [ 5, 34] as well as metabolic dysfunction with up to a 100% incidence rate can occur [ 3436]. Enterocystoplasty (gastrocystoplasties and ileocystoplasties) increases the risk of small bowel obstruction with a rate up to a 3.2–10.3% [ 5, 37, 38]. Bladder perforation rate ranges from 2 to 8.6% [ 5]; additionally, spontaneous bladder rupture can occur in 3% and is connected to poor catherization compliance [ 25]. Excessive mucous production seems to occur more frequently after colocystoplasties and less frequently after ileocystoplasties and gastrocystoplasties [ 34, 39, 40].
Renal scarring and chronic renal failure in patients who undergo augmentation cystoplasty poses a long-term complication that seems to be linked to incompliance with self-catherization as well as catherization per urethra [ 25].
The implementation of an urothelium-like tissue might avoid such short-and long-term adverse effects (Table  1). Moreover, a high level of elasticity, a good compliance to high and rapid changes of the affecting pressure would be essential requirements to the used tissue. In addition, the potential development of a malignant degeneration of the used tissue should be excluded.

Animal testing in experimental bladder augmentation

Naturally derived biomaterials
  • Fascia and muscle grafts (Table  2)
    Experimental bladder augmentation with muscle or muscle-backed flaps has been done as early as the beginning of the last century. In 1917, Neuhof performed bladder augmentation in dogs utilizing free fascia grafts [ 41]; details on the outcome are not available.
    Several experimental animal studies have since been performed on muscle-backed peritoneum, as well as rectus abdominis muscle flaps in rats [ 42]. Weingarten et al. found an increase in bladder volume in dogs after myoperitoneocystoplasty [ 43]. Manzoni et al. performed augmentation cystoplasty in thirty rats using rectus abdominis grafts, but bladder stones, chronic inflammatory response at sutures sites as well as undesirable residual muscle contractility occurred [ 42].
  • Demucosalized intestinal tissue (Table  3)
    Since the 1980s, animal studies (rats, calves, rabbits and pigs) focussing on using demucosalized colonic tissue and small intestine have been performed. Weingarten et al. found increased bladder volumes as well as urothelial growth [ 43].
    Oesch et al.. [ 44] performed augmentation cystoplasty using stripped coecum and reported urothelial growth in only approximately half of the test rats after 4 months [ 44]. Motley et al. described urothelial growth in 10 out of 11 calves after sigmoidocystoplasty, but residual intestinal mucosa and graft diverticulation occurred [ 45]. Niku et al. showed incomplete urothelial growth in rabbits after colocystoplasty, leading to postoperative demise of several test animals due to inflammation [ 46]. Clementson Kockum et al. stated that de-epithelialized colocystoplasty leads to graft contraction, fibrosis and metaplasia in a study done on 21 piglets [ 47].
    Burgu et al. tried to overcome the side effects of ileocystoplasty by either adding gastric tissue or by performing reversed in situ ileocystoplasty in rats. There was no improvement in terms of metabolic imbalances and stone formation following gastroileocystoplasty and ileocystoplasty [ 48].
  • Other autologous tissue (Table  4)
    Thangappan et al. successfully performed augmentation cystoplasty in 12 rats using de-epithelialized bladder wall grafts, although chronic inflammation as well as residual donor urothelial cells were found [ 49].
    Although augmentation with live-related-donor bladder grafts in rats showed promising results, transferring this particular two-step procedure to humans appeared difficult, as stated by Yamataka et al. [ 50].
    Ureterocystaugmentation was performed successfully in pigs, but only after iatrogenic creation of megaureters as reported by Ikeguchi et al. [ 51].
    Human dura mater, stomach and de-epithelialized small intestine tissue were used in augmentation cystoplasty in rabbits performed by Cranidis et al. The grafts covered iatrogenic bladder diverticuli following dertrusorectomy. The best results were obtained by using small intestine, although remnant intestinal mucosa was described. Graft contraction as well as bladder stones and fibrosis occurred in the groups with use of de-epithelialized gastric tissue and dura mater [ 52].
    To bypass risks and complications affiliated with gastric or intestinal resection, pedicled gastrocystoplasty was performed in a rodent model in 2004. Unfortunately, this method showed a number of side effects such as bladder calculi, metaplasia, passing of the test animal as well as scarring [ 53, 54].
    Dapena et al. demonstrated that hysterocystoplasty entails less adverse effects in animal studies than conventional enterocystoplasties in terms of metabolic imbalances and bladder calculi. However, smooth muscle cells were found to be sparse and there was evidence of fibrosis leading to obstruction [ 5557].
    In a rat model, human amniotic membranes were successfully tested as hypoallergenic grafts, but the bladder capacity did not increase after application of amniotic membranes for augmentation because of the small size of the defect in the bladder wall and graft [ 58].
Table 2
Fascia and muscle grafts in experimental bladder augmentation
Year
Author
Animal
Graft material
Adverse effect
1917
Neuhof [ 41]
Dogs
Muscle fascia
1990
Weingarten et al. [ 43]
Ferrets
Myoperitoneal pedicle flap
Bladder stones
2001
Manzoni et al. [ 42]
Rats
Autoaugmentation and muscle flaps
Bladder stones, chronic inflammation
Table 3
Demucosalized intestinal tissue in experimental bladder augmentation
Year
Author
Animal
Graft material
Adverse effect
1988
Oesch et al. [ 44]
Rats
De-epithelialized coecum
Incomplete urothelial coverage
1990
Motley et al. [ 45]
Calves
Sigmoid
Graft diverticulation, residual intestinal mucosa
1995
Niku et al. [ 46]
Rabbits
Colon
Postoperative mortality, inflammation
1999
Clementson Kockum et al. [ 47]
Piglets
De-epithelialized colon
Graft contraction, fibrosis, metaplasia
2011
Burgu et al. [ 48]
Rats
Ileum, gastric tissue
Metabolic imbalances, bladder stones
Table 4
Various types of tissue used in experimental bladder augmentation
Year
Author
Animal
Graft material
Adverse effect
2012
Thangappan et al. [ 49]
Rats
De-epithelialized bladder wall grafts
Chronic inflammation, residual donor cells
2003
Yamataka et al. [ 50]
Rats
Bladder wall grafts
Two-step procedure and immunosuppressants may be required
1998
Ikeguchi et al. [ 51]
Pigs
Ureteral tissue
Megaureter required
1998
Cranidis et al. [ 52]
Rabbits
Human dura mater, de-epithelialized small intestine and gastric tissue
Residual intestinal mucosa, stomach perforation, graft contraction
2004
Aslan et al. [ 53]
Rat
Pedicled gastric tissue
Bladder stones, metaplasia, postoperative mortality, scarring
2012, 2013
Dapena et al. [ 55, 56]
Rat
Uterus
Fibrosis
2017
Barski et al. [ 58]
Rat
Human amniotic membrane
No increase in capacity
Cell-seeded biological grafts
Studies investigating cell-seeded biological grafts are outlined in Table  5.
Table 5
Seeded de-epithelialized intestinal tissue in experimental bladder augmentation
Year
Author
Animal
Graft material
Adverse effect
2001
Blanco Bruned et al. [ 59]
Rats
Seeded intestinal grafts
No increase in capacity
2005
Hafez et al. [ 60]
Pigs
Seeded demucosalized colon
No information on results with neuropathic bladder cells
2015
Hidas et al. [ 61]
Pigs
Seeded demucosalized colon
No information on results with neuropathic bladder cells
2004
Fraser et al. [ 62]
Minipigs
Seeded de-epithelialized uterine tissue/colon
Incomplete urothelial coverage, graft contraction, fibrosis
2011
Turner et al. [ 63]
Pigs
De-epithelialized colon, urothelium sheets
Graft shrinkage
Schaefer et al. succeeded in transferring urothelial cells to colon and gastric grafts in vitro. However, they did not perform augmentation cystoplasty in vivo [ 64].
No increase in postoperative bladder volume was found following intestinal grafts seeded with urothelium in rats as demonstrated by Blanco Bruned et al., which resulted in a high mortality rate of 63.3% [ 59].
Seeding colonic grafts with urothelial cells and smooth muscle cells with an aerosol spraying technique was developed in 2003 [ 65]. Two ensuing studies showed the effectiveness of this bladder augmentation method in terms of cell adhesion and confluent epithelial coverage, although smooth muscle cell growth occurred only after an additional adding of detrusor cells to the urothelial cells [ 60, 61]. Hafez et al. compared aerosol transfer of smooth muscle cells onto demucosalized colon grafts to conventional colocystoplasty and found complete urothelial coverage only in the animals that underwent the aerosol graft cystoplasty [ 60]. Hidas et al. showed similar results, with no fibrosis or inflammation in porcine cystoplasty using the aerosol transfer technique. However, Hidas et al. stated that further studies in animals with neuropathic bladder should be done, as the results in a neuropathic bladder population might deviate [ 61].
Incomplete urothelial covering of seeded de-epithelialized uterine tissue derived from minipigs was reported in an experimental cystoplasty study done by Fraser et al., as well as graft contraction and fibrosis in de-epithelialized colonic tissue. [ 62].
Turner et al. successfully combined urothelium sheets with de-epithelialized colon tissue in a porcine model, but described graft shrinkage [ 63].
  • Acellular matrix grafts (Table  6)
    Biomaterials such as acellular matrix grafts and bladder submucosa collagen matrix have been used successfully in animal trials because of their good biocompatibility [ 66]. However, acellular bladder matrix grafts do not promote the ingrowth of smooth muscle cells and there is therefore no structural integration. Postoperative urinoma and urinary tract infection can occur as well, and antigenicity cannot be precluded completely [ 6770].
    Kropp et al. described complete urothelial graft overgrowth in 22 rats after cystoplasty with porcine-derived small intestinal submucosa (SIS); however, there were bladder calculi, leakage, inflammation and incomplete smooth muscle cell growth noticed [ 71].
    Parshotam Kumar et al. reported on the evidence of fibrosis with SIS in augmentation cystoplasty in lambs [ 72].
    Sharma et al. seeded stem cells unto de-epithelialized small intestine tissue and used the graft to perform augmentation cystoplasty in primates, showing urothelial and smooth muscle growth but no increase in postoperative bladder volume [ 73].
    By managing to perform a bladder augmentation using only smooth-muscle cells sheets, Talab et al. showed that neovascularization and epithelialization can be achieved without the use of a scaffold. However, there was no testing regarding the postoperative bladder volume. [ 74].
    Muscle cell migration could also be enhanced by seeding acellular bladder grafts with adipose-derived stem cells, as demonstrated by Zhe et al., although bladder calculi and insufficient smooth muscle cell growth occurred [ 75].
    Smooth muscle cells harvested from neuropathic bladders showed similar results to matrices seeded with normal cells when seeded unto matrices in vitro and then transplanted in vivo [ 76, 77]. This adds a new perspective to the findings of Subramaniam et al., who found that urothelial cells harvested from patients with bladder dysfunction showed reduced proliferation and differentiation [ 78].
  • Polymers, collagen grafts, glycosaminoglycans (Table  7)
    Nano-structured polymers have been tested since 2007, providing adequate surface properties for smooth muscle and urothelium proliferation. However, death as a consequence of bladder leak was reported as well as untimely biodegradation, sparse smooth muscle cell growth, fibrosis as well as no increase of the bladder capacity [ 79, 80]. However, seeded polymer grafts did not show these adverse effects as shown by Kwon et al. [ 80]. Parshotam et al. found that augmentation cystoplasty using INTEGRA® (INTEGRA LIFE SCIENCE CORPORATION, Plainsboro, New Jersey, USA) collagen matrix showed better results than SURGISIS® (COOK, Spencer, Indiana, USA) collagen matrix or demucosalized enterocystoplasty in lambs. Mucous cysts as well as intestinal obstruction, fibrosis and graft shrinkage were described in the enterocystplasty as well as in the SURGISIS® (COOK, Spencer, Indiana, USA) groups [ 72].
    Zhou et al. advanced the use of tissue-engineered grafts by applying vascular endothelial growth factor and platelet-derived growth factor onto bladder acellular matrices to enhance muscle and vascular ingrowth. While the bioactive factors did promote smooth muscle cell regeneration and neovascularization, urinary leakage and bladder stone formation occurred, as well as graft shrinkage, scarring and graft calcification [ 81].
    Further experimentation by Vardar et al. on collagen–fibrin scaffolds showed improved urothelialization and smooth muscle cell growth by adding insulin-like growth factor. Nonetheless, there was hypertrophy of the constructed urothelium which could lead to outlet obstruction [ 82].
    In a recent study from 2017, unseeded and seeded cystoplasty collagen grafts were compared, with inconsistent results regarding the ingrowth of urothelial and smooth muscle cells [ 83].
Table 6
Acellular matrix grafts in experimental bladder augmentation
Year
Author
Animal
Graft material
Adverse effect
1995
Kropp et al. [ 71]
Rats
SIS
Bladder stones, inflammation, leakage, inflammation, incomplete smooths muscle cell growth
2010
Parshotam Kumar et al. [ 72]
Sheep
SIS
Fibrosis
2011
Sharma et al. [ 73]
Primates
Seeded SIS with stem cells
No increase in capacity
2014
Talab et al. [ 74]
Rabbits
Smooth-muscle cell sheets
Fibrosis, no information on postoperative bladder capacity
2016
Zhe et al. [ 75]
Rats
ACS-seeded acellular bladder grafts
Bladder stones, insufficient cell growth
SIS small intestinal submucosa, ACS adipose-derived stem cells
Table 7
Polymers, collagen grafts, glycosaminoglycans in experimental bladder augmentation
Year
Author
Animal
Material
Adverse effect
2007
Pattison et al. [ 79]
Rats
Polymer scaffolds
Bladder leak, bladder stones postoperative mortality, slow biodegradation, mechanical difficulties
2008
Kwon et al. [ 80]
Dogs
Polymer scaffold
Chronic inflammation, rapid scaffold degradation
2010
Parshotam Kumar et al. [ 72]
Lambs
Collagen scaffolds (INTEGRA® [INTEGRA LIFE SCIENCE CORPORATION, Plainsboro, New Jersey, USA], SURGISIS® [COOK, Spencer, Indiana, USA])
Fibrosis, graft contraction
2013
Zhou et al. [ 81]
Rabbits
Acellular bladder matric and growth factors
Bladder stones, graft shrinkage/calcification/scarring, urinary leakage
2016
Vardar et al. [ 82]
Collagen–fibrin scaffold and IGF-1
Possible outlet obstruction because of tissue hypertrophy
2017
Leonhäuser et al. [ 83]
Minipigs
Unseeded and seeded collagen scaffolds
Inconsistent cell ingrowth, risk of leakage
Synthetic materials
Synthetic materials which have been employed in experimental bladder augmentation are presented in Table  8.
Table 8
Synthetic materials in experimental bladder augmentation
Year
Author
Animal
Material
Adverse effect
1957
Kudish [ 84]
Dogs
Polyvinyl sponges
Foreign body reaction
1970
Kelâmi et al. [ 85]
Dogs
Teflon® (BARD INC., Murray Hill, New Jersey, USA) felt
Fibrosis, incomplete urothelial coverage, no smooth muscle cell growth, graft collapse
1994
Virseda Chamorro et al. [ 86]
Dogs
Gore-Tex® (W.L. GORE and ASSOCIATES, INC., Flagstaff, Arizona, USA)
No increase in capacity
Polyvinyl sponges [ 84], Teflon® (BARD INC., Murray Hill, New Jersey, USA; [ 85]), as well as Gore-Tex® (W.L. GORE and ASSOCIATES, INC., Flagstaff, Arizona, USA); patches [ 86] have been used in experimental animal studies, too. However, there was no increase in capacity due to the stiffness of the material and no ingrowth of muscle cells [ 86]. Moreover, foreign body reactions, fibrosis, incomplete urothelial growth as well as no smooth muscle cell ingrowth have been described [ 84, 85].
Silk-based scaffolds
Silk-based scaffolds which have been used in experimental bladder augmentation are shown in Table  9.
Table 9
Silk scaffolds in experimental bladder augmentation
Year
Author
Animal
Material
Adverse effect
2013
Seth et al. [ 87]
Rat
Silkworm silk scaffold/combined with SIS
Foreign body reaction
2014
Chung et al. [ 88]
Rat
Silkworm silk fibroin scaffolds combined with SIS
Bladder stones, bladder rupture, chronic inflammation, residual silk
2015
Zhao et al. [ 66]
Rat
Silkworm silk combined with acellular bladder matrix graft
No increase in capacity
2013
Tu et al. [ 89]
Pigs
Acellular silkworm silk scaffolds
Urinary leakage, bladder calculi, graft contraction
SIS small intestinal submucosa
To facilitate the growth of urothelial and smooth muscle cells, grafts have been lined with silkworm silk ( Bombyx mori). However, Seth et al. described a high incidence of foreign body reaction in either silk matrices or small intestinal submucosa combined with silkworm silk [ 87]. Chung et al. found regrowth of smooth muscle cells by combining small intestinal submucosa and silkworm silk in a rat cystoplasty model, but again, bladder stones and bladder rupture as well as chronic inflammation and residual silk were present [ 88]. Zhao et al. used silkworm silk to line a bladder acellular matrix graft in rats. Although there was ingrowth of smooth muscle cells present, bladder stones as well as graft perforation and chronic inflammatory response occurred [ 66]. Tu et al. tested acellular silkworm silk scaffolds in pigs, and although smooth muscle cells as well as nerve cells and neovascularisation were successful, urinary leakage as well as urinary calculi and graft contraction still ensued [ 89].
Due to the fact of current inflammation, stone production, leakage and persistence of silk graft remnants, this particular method for bladder augmentation needs to be further investigated. Presumably, a more suitable silk donor has to be found to eliminate these adverse effects such as antigenicity and formation of calculi.

Conclusion and perspective

In conclusion, the implementation of tissue and neo-organs fabricated in vitro seems feasible in partial or total organ reconstruction. Seeded biomaterials (collagen, keratin, alginate, acellular tissue matrices, synthetic polymers) surpass non-biomaterials (Teflon® [BARD INC., Murray Hill, New Jersey, USA], silicone, Vicryl® [ETHICON INC., Cincinetti, Ohio, USA], polyvinyl, unseeded collagen matrices) in terms of biocompatibility, degradation, cell adhesion substrate, tissue development, mechanical and physical properties as well as plasticity.
The best results in seeding the grafts are obtained by using autologous urothelial and smooth muscle cells.
Research concerning the use of stem cells, amniotic fluid and progenitor cells from urine as well as “printing” 3D scaffolds in vitro is still ongoing [ 76, 77, 90].
Minimizing or alleviating the ailments of congenital malformations or traumatic injuries of the urinary tract by operative means remains a challenge for paediatric surgeons as well as for interdisciplinary carers.
New techniques and possibilities in the operating field of bladder augmentation and ureteral reconstruction give new future perspectives in terms of reducing side effects and maximizing the quality of life of the afflicted patients.

Conflict of interest

S. Langer, C. Radtke, E. Györi, A. Springer and M.L. Metzelder declare that they have no competing interests.
Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://​creativecommons.​org/​licenses/​by/​4.​0/​), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

Unsere Produktempfehlungen

Abo für kostenpflichtige Inhalte

Literatur
Über diesen Artikel

Weitere Artikel der Ausgabe 3-4/2019

Wiener Medizinische Wochenschrift 3-4/2019 Zur Ausgabe