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14
R. Shi et al.
somatic nerves. The vascular system is also
bounded by this. There is an internal hemorrhoidal venous plexus that injects into the superior rectal artery upward, and an external
hemorrhoidal venous plexus that ows to the
middle and inferior rectum veins downward
(Fig.2.2). The return of lymph uid also serves
as the dividing line, but it is not absolute.
Malignant tumors in the anal canal can move up
to the root of the inferior mesenteric artery, laterally to the pelvis, and lower to the groin.
The dentate line is the dividing line between
the internal and external hemorrhoids, and the
branches of the joint longitudinal muscles,
which Parks calls the so-called mucosal suspensory ligament, are attached here to distinguish the rectum from the anus. The epithelium
is also divided into two parts: the upper part is
the submucosal space, which contains the
internal hemorrhoidal venous plexus, and the
lower part is the perianal space, which contains
the external hemorrhoidal venous plexus.
There is very little blood ow between these
two spaces. When swelling occurs, although
the upper and lower parts are swollen, the
boundary is xed and causes blood circulation
obstacles. Therefore, when the hemorrhoids
are incarcerated, a deep groove can be seen
there.
The shape of dentate line is a zigzag, and the
upper part of the upward protruding area is the
anal column, and the anal column has a rectal
column of Morgagni (Fig. 2.3), of which there
are about 8 to 14. The sunken between the anal
columns is called anal sinus, and the epithelium
on its lower edge is pocket-shaped or bowlshaped, called the anal valve. The protruding part
on the tooth line is called the anal papilla. When
the anal papilla grows due to chronic inammation, it is called anal papillary hypertrophy, also
known as anal polyps.
The sunken on the inside of the anal ap is
called an anal recess, also referred to as an anal
sinus. The Italian anatomist Giantatista
Morgagni (1682–1771) rst recorded anal
crypts. The number of anal crypts ranges from 6
to 11 (8 on average), with the anus being the
deepest at 1.0 mm, the front depth being 0.7
mm, and the left and right sides being 0.4mm.
Inammation here is known as anal cryptitis,
and its symptoms are persistent mild to moderate pain. When the anal crypt is inamed, mild
tenderness and induration can be palpated on
the anal crypt using a digital examination. About
65% of anal crypts have an opening at the bottom of the anal gland, which is connected to the
anal gland through an anal gland duct (Fig.2.4).
For ease of understanding, sometimes it is
Pelvic
lymph nodes
Lymph
Inguinal
lymph nodes
Fig. 2.2 The anatomical and clinical signicance of dental line
Superior rectal
artery and vein
Blood
Supply
Middle and lower
rectal arteries
and veins
Autonomic
Nervous
System
Nerves
Spinal
Nerves
Dentate
Line
Columnar
epithelium
Epithelial
Tissue
Squamous
epithelium
Endoderm
Origin
Ectoderm
nal Anal Sphincter
Pe
Upper rectal valve
Internal anal sphincter
External Anal Sphincter
(Subcutaneous)
2 Anatomy andPhysiology ofAnal Fistula
Mid rectal valve
ritoneal reflection
15
Internal rectal ring muscle
External longitudinal
muscle of rectum
Lower rectal valve
Fig. 2.3 Anal canal and rectum
Fig. 2.4 Anal gland and
anal crypt
Anal transitional section
Anal crypt
Dentate
Line
Anal
valvulae
Anal Verge
Columns of
Morgagni
External Anal Sphincter
(Subcutaneous)
Anal intersphincteric groove
Levator Ani M.
Exter
(Deep)
External Anal Sphincter
(Superficial)
Dentate Line
Rectum
Anal canal
External Anal Sphincter
(Deep)
Internal anal sphincter
External Anal Sphincter
(Superficial)
Anal Gland
16
R. Shi et al.
divided into three zones according to the four
boundaries of the anal canal, namely the four
lines and three zones (Fig.2.1).
The four lines are the anal skin line, the anal
white line, the dentate line, and the anorectal line.
The anal skin line is the anal margin. The anal
white line is equivalent to the boundary between
the lower edge of the internal sphincter muscle
and the underside of the external sphincter skin,
that is, the position of the inter sphincteric grove.
Because there are fewer blood vessels in this
area, it may appear slightly off-white in some
people. The anorectal line is the horizontal line of
the upper edge of the anorectal ring, is located
above the dentate line, about 1.5 cm from the
dentate line, and is an imaginary line of the upper
end of the rectal column.
The three zones are the column band, the
hemorrhoid band, and the belt. The column band
is the ring zone from the anorectal line to the
dentate line. There is an anal column (i.e. rectal
column) in between, and the surface is covered
with a single layer of columnar epithelium. The
hemorrhoid band is the ring zone from the dentate line to the white line of the anus. The sphincter is compressed into a ring-shaped bulge,
where the surface is smooth and bright, and it is
the transitional part of the mucous membrane
and the skin. The dentate line changes from a
single columnar epithelium to a stratied cubic
epithelium and unkeratinized squamous (stratied at) epithelium. The belt is the ring-shaped
area from the white line of the anus to the edge
of the anus, surrounded by the lower part of the
external sphincter skin, and the surface is keratinized stratied squamous (stratied at)
epithelium.
Research by Gao Chunfang and Guo Maolin
found that on MRI images, there is a clear anatomical interface between the rectum and its
continuation and the pelvic oor; the anal canal
can be divided into two parts: the anal canal
and the perianal. It is composed of mucosal
layer, submucosal layer, and anorectal smooth
muscle layer. The rest is called the perianal
region.
2.2.2 Rectum
The rectum is located above the anal canal and is
about 10–15cm long. It is connected to the sigmoid colon at the top and the anal canal at the
bottom. The rectum descends along the front of
the sacrum and coccyx and forms an angle of
nearly 90° with the anal canal, called the anal
right angle. The upper and lower ends of the rectum are narrow, and the middle is enlarged, called
the rectal ampulla. Dilatation (rectal constipation), inammation (ulcerative colitis, Crohn’s
disease), spasm (irritable bowel syndrome), and
other diseases occur in the rectal ampulla. The
upper part of the rectum migrates to the sigmoid
colon, and its transition part is called the rectosigmoid junction (rectosigmoid) (Fig.2.5).
There are three semi-moon-like rectal valves
(rectal valves) on the rectal wall, which are called
the upper rectal valve, the middle rectal valve,
and the lower rectal valve. The lower rectal valve
is about 5 cm from the anus, the middle rectal
valve is about 8cm from the anus, and the upper
rectal valve is about 11cm from the anus. The
lower, middle, and upper rectal valves are located
on the left, right, and left sides, respectively. The
mid-rectal valve is called the Houston valve and
is equivalent to the height of the peritoneal reex.
When treating rectal lesions above the Houston
valve, it is easy to cause perforation to the
abdominal cavity. PPH surgery in China may
lead to perforation of the rectum and even death
of the patient. Special attention should be paid to
this.
The mucosal epithelium of the rectum is the
columnar epithelium. The rectum is divided into
the rectal mucosa, the inner ring muscle, and the
outer ring muscle from inside to outside. The
upper rectum is covered with peritoneum on the
front and both sides, and the middle section is
covered with peritoneum only on the front, and
here it turns back into a rectovesical pouch or rectovaginal pouch. The distance between the peritoneal reex and the anal margin is about 7.5cm
in men and 5.5cm in women. Fascia surrounds
the rectum below the peritoneal reex.
1. Column Belt
2. Hemorrhoid Belt
3. Skin Belt
4. Surgical Anal Canal
5. Anatomical Anal Canal
6. Sigmoid colorectal junction
7. Upper rectal valve
8. Mid rectal valve
9. Peritoneal reflection
10. Lower rectal valve
Anorectal Ring
2 Anatomy andPhysiology ofAnal Fistula
1
2
3
17
6
7
8
9
10
Dentate Line
4
5
Pectinate line
Anal Verge
Fig. 2.5 Anal canal and rectum
The rectal mucosa is thick and rich in blood
vessels. The mucosa is smooth, pink, and transparent, and large and small blood vessels in the
submucosa can be seen. This characteristic “vascular morphology” disappears in patients with
inammatory diseases and melanosis. The rectal
submucosa is loose and easily separated from the
muscle layer and prolapses downward.
The rectal venous plexus is already formed
under the rectal mucosa above the dentinal line
when humans are born. With aging, the rectal
venous plexus gradually expands and exes and
can develop into internal hemorrhoids. The
venous plexus of external hemorrhoids exists in
a ring shape at the anal margin and can develop
into external hemorrhoids (Fig.2.6). Because it
is between the skin and the sphincter, the terminal bers of the joint longitudinal muscle divide
it into many small gaps (Compartment).
Therefore, it is easy to produce blood circulation
disorder and form thrombus. Such thrombus formation is accompanied by pain because it is
located in the area where the sensory nerves are
distributed.
18
External hemorrhoid venous plexus
Conjoined
longitudinal
muscle
Superior rectal
n
R. Shi et al.
Right superior rectal vein
Fig. 2.6 Blood supply of hemorrhoids
vein
Superior rectal artery
Left superior rectal vei
Internal hemorrhoid
venous plexus
The rectal muscle layer is an involuntary muscle, the outer layer is the longitudinal muscle, and
the inner layer is the circular muscle.
In the front of the rectum, men have their
prostate, seminal vesicles, vas deferens, bladder, and rectovesical pouch, and women have
vaginas, cervix, uterus, and rectovaginal pouch
(Fig.2.7). There is the sacrum and the coccyx
behind the sacrum. Blood vessels and the hypogastric nerve plexus on both sides are the sciatic
bone, internal iliac artery, sciatic nerve, and
ureter.
2.3 The Anal Gland
2.3.1 The History ofUnderstanding
theAnal Glands
In 1878, Hhiari of Germany rst proposed the
name of “anal gland.” This structure was conrmed histologically by Hemauu and Desfosser
in 1880, but they called it the “migratory intesti-
nal gland.” This was followed by F.D. Johson
(1914, 1917) who used a large amount of materials to study the development of human embryos
at various stages and further elaborated on the
structure and location of anal glands and corrected the misconception that anal crypts are anal
glands. British H.·A.·Harris (1929) also conducted further research and reports on the anal
glands. In 1929, Lokhart-Mummery published a
paper on the structure of anal glands and their
relationship with infections around the anus. His
understanding was valued by the medical profession at that time and was used clinically for the
German medical community at that time.
However, it should be noted that in 1933 the
etiological relationship between the anal gland
and anal gland duct infection and perianal abscess
and anal stula was clearly recognized and valued in clinical practice. In 1993, Tucker of the
American Academy of Proctology made a pathological anatomical observation on the structure of
anal glands. The relationship between anal glands
and anorectal inammatory diseases was clearly
Anococcygeal Ligament
External Anal Sphincter
Genitour
2 Anatomy andPhysiology ofAnal Fistula
Rectovesical
pouch
Pubic
Prostate
L
5
S
1
S
Rs
2
Ra
Rb
Anal
Canal
Denonvilliers Fascia
Bulbocavernosus Muscle
19
S
3
S
4
S
5
C
0
Levator Ani M.
Anococcygeal Ligament
Puborectalis Muscle
External Anal Sphincter
External Anal Sphincter
L
5
External iliac
S
1
vein
Internal iliac vein
Ovaries
Rs
S
Oviduct
Round ligament
of uterus
Pubic
Ra
Rb
inary septum
Rectovaginal septum
Vaginal
Anal Canal
Fig. 2.7 Adjacent organs of the anorectum (male and female sagittal planes)
claried so that the anal gland and its clinical signicance were quickly paid attention to by more
clinicians. In 1961, A. G. Parks proposed the
theory of cryptoglandular infection on the mechanisms of anorectal infection. Parks believed that
most anorectal abscesses and anal stulas are
Uterine rectal
depression
2
S
3
S
4
S
5
C
0
Posterior fornix
of vagina
Levator Ani M.
Denonvilliers Fascia
Puborectalis Muscle
External Anal
Sphincter
20
R. Shi et al.
caused by anal gland infection, and most anal
gland infections originate from primary infections in the anal cryptsnal gland. Anal infections
caused by blood and lymphatic circulation are
generally rare. This study has been accepted or
applied by most scholars and clinicians at home
and abroad.
In my country, long before Parks put forward
the “cryptic gland infection theory,” the relationship between anal glands and the peri-anorectal
abscess has been recognized and used to guide
clinical practice. For example, Zhang Qingrong’s
report in 1957, based on his understanding that
peri-anorectal infections all originate from infections of the anal glands and that their internal
openings are mostly at the infected anal sinuses,
proposed that the key to the treatment of anal stula lies in the treatment of the infected foci of the
anal glands. He reported 674 cases of anal stula
that were treated between 1951 and 1955, and the
cure rate was as high as 98.8%.
In Japan, the understanding of anal glands and
their clinical signicance came relatively late and
was tortuous. Although in 1907 the Osawa clan,
followed in 1909 by the Taguchi clan and in 1931
the Ito Kazuki clan, Kono, Hashimoto, Shinkami,
and Kagawa clan etc. all have done research into
anal glands, they have all ignored the clinical signicance of anal glands. At that time in Japan, as
for the mechanism of peri-anorectal infection,
some believed that it was mainly caused by bacterial invasion after rectal mucosal injury, some
believed that it was mainly caused by tuberculosis infection, and some believed that it was caused
by the anorectal wall or local infection of tuberculosis lesions.
2.3.2 The Distribution ofAnal
Glands andTheir Clinical
Signicance
Regarding the distribution of anal glands around
the anus, some people think that in children under
ve years old, they are irregular, while in adults,
they are mostly concentrated near the posterior
midline of the anal canal (84%), with less on both
sides. However, it is believed that most of the
anal glands are located in the posterior center,
rarely in the anterior center, and none on both
sides. Chen Qinglan, Jin Meifang, and others
pointed out after observing 12 cases of anal canal
and rectal specimens by continuous sectioning
that 58% of the anal glands are located in the posterior half of the anal canal, and 42% of the anal
glands are located in the front half of the anal
canal.
In terms of clinical reports, many reports
pointed out that the internal opening of anorectal
abscess and anal stula are located at the opening
of the anal gland on the back of the anus. According
to the observation of Sumikoshi, most of the stulas of the ischiorectal fossa are caused by the formation of infection in the anal crypts on the back
of the anus, and the inammation further spreads
to the ischiorectal fossa on both sides. Anal stulas
formed by anal gland infections in other parts
rarely spread to other spaces even if they are
infected again. If the infection starts in the posterior midline anal gland, it will form low and high
intermuscular stula and is easy to develop into
ischiorectal fossa stula. However, Sumakoshi
believes that this is because the anal crypt in the
middle of the anus is deeper, and there are more
opportunities for fecal dirt to enter the anal crypt.
Some people think that anal cryptitis usually
occurs in the posterior center and is related to the
following factors: (1) the number of crypts in this
area is large and obvious; (2) the posterior center
of the anus is the weakest resistance in the tricyclic system of the external sphincter; and (3) the
inferior rectal artery does not form arterial
branches at the joint behind the anus, and the
blood supply is relatively poor.
According to Wang’s statistics, 68.6% and
69.7% of perianal abscesses and anal stulas
have the internal orice behind the anus, with
relatively few on both sides.
In short, the current understanding of the
plane distribution of anal glands around the anus
is still inconsistent.
Regarding the distribution of anal glands
above and below the dentate line, Fujihara Akira
pointed out through the morphological study of
the anal recesses, anal glands, and anal glands of
Japanese people that 65% of the anal gland ducts
2 Anatomy andPhysiology ofAnal Fistula
21
are arranged perpendicular to the dentate line, not
with the dentate line. The vertical accounted for
35%, of which 28% had the catheter running
under the dentate line and 4% were partly on the
dentate line and partly under the dentate line.
Zhou Liangyou et al. pointed out that the anal
glands are mainly located near the dentate line
and are distributed in the submucosa. A portion
of the anal glands enters the internal sphincter,
and none enters the external sphincter.
The understanding about the extension direction and distribution range of anal glands is also
inconsistent. Eisenhammer in 1957 and Parks in
1961 reported that the vast majority of anal
glands penetrated the internal sphincter and then
traveled between the internal and external sphincter and did not distribute to the joint longitudinal
and external sphincter. However, it was also
pointed out that the anal gland can penetrate into
the external sphincter, ischiorectal fossa, and
levator ani to the pelvic cavity. Zhou Liangyou
and Zhang Dongming also believed that the anal
ducts are mostly conned to the submucosa in
children and penetrate the internal sphincter in
adults. It can reach as far as the junction between
the internal sphincter muscle and the joint longitudinal muscle, and no further extension is found.
He also believed that this situation can be
explained by the genesis of the anal canal, that is,
the anal canal is composed of two components of
internal organs and the body, but is not intertwined, so the anal glands belonging to the visceral component cannot penetrate deeply into the
external sphincter and the body component
within the levator ani muscle. Therefore, it is
considered that the report on the long-stroke anal
duct is questionable.
The extensive direction and scope of anal
glands are of great signicance to the formation
and treatment of anorectal infections. Based on
the knowledge that the anal glands are mainly
located in the internal and external sphincter, statistics found that 97% of perianal abscesses and
anal stulas occur between the internal and external sphincter, and a theory of “interanal stula
abscess” was put forward on the mechanism of
perianal abscess. The idea of preserving the
sphincter to cure anal stula based on the distri-
bution characteristics of the anal glands was also
put forward and put into practice. However, due
to insufcient treatment of the primary intermuscular lesions, the recurrence rate is high. This surgical method of preserving the anal sphincter to
cure anal stula was the rst success for Parks. At
present, the radical operation of anal stula and
peri-anorectal abscess preservation anal sphincter at home and abroad has also been proposed
and developed based on Eisenhmmer and Parks’
understanding of the structure and distribution of
anal glands.
2.3.3 The Shape andClinical
Signicance ofAnal Glands
In order to further clarify the relationship between
anal stula and anal glands, Japanese scholars
such as Akio Kurokawa and Hirokawa Kurokawa
divided the anal glands into anal stula group and
nonanal stula group for histopathological observation. Through the serial section and observation of the parafn specimens of 41 cases of anal
stula group and 37 cases of nonanal stula
group, it was found that the anal glands consisted
of glands and ducts opening in the anal crypts,
which were divided into the straight type and the
curved type according to different shapes. The
glandular room type is composed mainly of glandular rooms; the mixed type has equal proportions of ducts and glandular rooms; and the cystic
type has mucus retained as cysts. In the nonanal
stula group, the most common type of anal
glands is duct-curved type, accounting for 37.9%,
followed by mixed type, accounting for 21.6%;
glandular room type, accounting for 18.9%; ductstraight type, accounting for 13.5%; and cystic
type, accounting for 8.1%. In the anal stula
group, most of the anal gland types were ductal
straight type, accounting for 85.3%, followed by
mixed type, accounting for 9.5%; duct curved
type, accounting for 4.9%; and glandular chamber type and cystic type not being found.
Compared with the non-anal stula group, there
are signicant differences between the two
groups in the types of anal glands. Further observation found that 78% of the anal stula group
22
R. Shi et al.
had a small amount of squamous epithelium in
the anal glands, while 24.3% of the nonanal stula group had a small amount of squamous epithelium. This is also very signicant. Furthermore,
Langerhaiis cells are often found in anal glands
mixed with at epithelium. As for why the anal
glands of the anal stula group and the nonanal
stula group have this difference and what their
clinical signicance is, they did not provide further explanation.
2.3.4 The Relationship Between
theObstruction ofAnal
Glands andtheOccurrence
andDevelopment
ofAnorectal Infections
Many scholars believe that the obstruction of
anal glands has a very important relationship
with the occurrence of anorectal abscess and anal
stula. Yasuo Yamamoto (1980) believed that
when the infected material enters the anal duct
from the anal crypt and then retrogrades from the
anal duct to the anal glands, the anal glands
become infected, and the inammation is aggravated due to the action of the acidic uid in the
glands. In turn, the gland cells are stimulated to
promote the secretion of mucin. The secretion of
mucin promotes further inammation, forming
an anal gland abscess, and part of the pus can be
discharged through the anal gland duct. However,
when this process occurs repeatedly, the inammation causes the adhesion and occlusion of the
anal gland ducts. The pus of anal gland abscesses
cannot be discharged through the anal gland
ducts and can only break through the surroundings, such as through submucosal and subcutaneous breakthroughs, or it will move along with the
movement of the muscles along the joint longitudinal muscle bers and spread up, down, left and
right, forming various perianal abscesses and
anal stulas. Especially when the anal glands are
within the internal sphincter or penetrate into the
internal sphincter to reach the intersphincter, the
anal glands are more likely to be blocked due to
muscle compression. Therefore, Yamamoto
believed that according to experience and pathol-
ogy, once the inammation spreads to the deep
part, the anal glands are occluded and no longer
communicate with the anal crypts. Therefore,
Yamamoto advocated retaining the anal canal
and rectal mucosa, including anal recesses, during anal stula surgery.
Eisenhammer believed that the primary anorectal recessed adenomyosis (intersphincter) stula abscess and every damage to the stula stem
from the spread of abscesses in the deep anal
gland or perianal space. The spread of the abscess
is due to obstructive infection of the duct that
connects the gland to the anal recess at the dental
line. At the same time, he also pointed out that
this view that only obstructive infections can
cause abscess formation is still controversial
because anal cryptitis caused by nonobstructive
infections is not uncommon, and infectious diarrhea and severe diarrhea are not uncommon disease factors.
As early as 1957, Zhang Qingrong pointed out
that anal duct obstruction is closely related to the
occurrence of anorectal abscess. He pointed out
that when stool passes through the anal canal, it
can sometimes send infectious material into the
anal sinus and then pass through the duct to infect
the anal glands. The infectious material accumulates in the ducts and acinars and nally causes
the ducts and glands to iname. The bubble
swells and ruptures so that the infectious material
directly invades the tissues around the anus and
rectum, or indirectly spreads through blood vessels or lymphatic vessels, and nally forms an
abscess around the anus and rectum.
Chen Qinglan etal.’s observation of 12 serial
sections of anal canal specimens showed that
there are closed glands in the deep layer of the
anal canal in adults, and it is not uncommon. This
kind of glandular cyst is mostly located at the end
of the glandular duct and near the joint longitudinal muscle. No open duct is found to connect to
the intestinal cavity, and there was even secretion
in the glandular cavity. They believe that this
kind of closed glandular cyst is one of the reasons
for the loss of ducts. Inammation causes internal sphincter spasm, oppresses the ducts, and
occludes them, causing the secretions of the anal
glands to be difcult to discharge, and thus cystic
2 Anatomy andPhysiology ofAnal Fistula
23
enlargement occurs. Once this saccular line is
infected, a primary abscess between the sphincter
will be formed. From a clinical point of view,
some people think that the inner orice of the
anorectal abscess is mostly occluded. The reason
may be the necrotic tissue has not liqueed and
blocked the anal duct; the tissue around the anal
duct is inamed and occludes the orice; and the
duct is in the sphincter. The perianal inammation causes sphincter spasm, which can in turn
cause twisting and occlusion of the duct and high
pressure in the abscess cavity of anal gland
abscesses, compressing the duct or internal opening to seal it.
Eisenhammer reported that in only one-third
of anal stula cases, the anal gland duct is connected to the inner wall of the anal duct.
2.3.5 The Relationship Between
Anal Glands andSex
Hormones andTheir Clinical
Signicance
As a skin urologist, Gao Yuejin in Japan found
that according to his observations in more than
50 years of clinical work, there is a clinical phenomenon that cannot be explained by the “anal
crypt gland infection theory” that there are almost
no babies in the early patient cases of anal stula.
There are two very similar peaks in the age distribution curve of male patients, adolescents, and
the elderly, and these are in the neonatal infant
period and the young adult period; the incidence
rates of male and female are signicantly different. The ratio of rates is 8–9:1, while in adults it
is 5–6:1. Whether it is a newborn baby or an
adult, male patients account for the vast majority
of cases; the occurrence of anal stula in a newborn baby tends to occur before the age of one
year, and most of the onset sites are on both sides
of the anus and are symmetrically distributed. In
addition, most males have stulas with more
branches compared to female patients. Based on
the genetic origin of the anal glands from the fat
glands, combined with research on the cypress
(showing that the adult anal glands are apocrine
glands, and their contents sometimes contain fat),
he speculated that the anal glands may also
resemble the fat glands, which are excellent target organ for hormones in males. However, the
author failed to directly and clearly explain the
role of male hormones in anal gland infections.
The article mainly describes the relationship
between fat glands and male hormones.
2.3.6 Histochemistry ofAnal Gland
Mucus andIts Clinical
Signicance
Research by Akio Kurokawa has shown that the
production and nature of anal gland mucus have a
certain relationship with the occurrence of anorectal infections.
Kurokawa found that the at epithelial metaplasia of the anal gland epithelium can lead to a
decrease in the ability of the anal glands to produce mucus, and the anal glands with at epithelial metaplasia accounted for 81.5% of the anal
glands in patients with anal stula. This meant
that they were atter than the anal glands in nonanal stula patients. The epithelial metaplasia
rate is 28% higher. At the same time, it was found
that the incidence of the squamous epithelium of
the anal glandular epithelium increased with age,
while the ability of the anal glands to produce
mucus also decreased or declined. Further studies
have shown that the anal gland epithelium
(mainly mucus-producing columnar epithelium
with a small amount of goblet cells) stained with
AB-PAS, HID-AB, a layer of thiomucin can be
found. This is true even in areas with squamous
metaplasia. When observing the afnity of phytohemagglutinin to the surface membrane, it was
found that some of the goblet cells were UEA-1
and PHA-positive, while the cell edges and cells
with squamous metaplasia were VEA-1-positive.
Therefore, it was believed that due to the at epithelial metaplasia of the anal gland epithelium,
the low ability to produce mucus is related to its
immune function.
In short, most scholars currently believe that
the anal glands play an important role in perianorectal infections. Once the anal glands are
infected, an abscess is formed between the inter-