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Long Walk to Freedom
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For other uses, see Long Walk to Freedom (disambiguation).
Long Walk to Freedom
Author
Nelson Mandela
Cover artist
Allan Tannenbaum
Country
United States
Language
English
Subject
Autobiography
Genre
Non-fiction
Publisher
Macdonald Purnell
Publication date
1994
Media type
Print (hardback and paperback)
Pages
630 pp
ISBN
0-316-87496-5
OCLC
39296287
Long Walk to Freedom is an autobiographical written by South African President Nelson Mandela, and first published in 1994 by Little Brown & Co.[1] The book profiles his early life, coming of age, education and 27 years in prison. Under the apartheid government, Mandela was regarded as a terrorist and jailed on the infamous Robben Island for his role as a leader of the then-outlawed ANC. He later achieved international recognition for his leadership as president in rebuilding the country's once segregated society.[2] The last chapters of the book describe his political ascension, and his belief that the struggle still continued against apartheid in South Africa.
Mandela dedicated his book to "my six children, Madiba and Makaziwe (my first daughter) who are now deceased, and to Makgatho, Makaziwe, Zenani and Zindzi, whose support and love I treasure; to my twenty-one grandchildren and three great-grandchildren who give me great pleasure; and to all my comrades, friends and fellow South Africans whom I serve and whose courage, determination and patriotism remain my source of inspiration."
Contents
[hide]
1 Overview
2 Reviews
3 Film adaptation
4 Ghost writer
5 See also
6 References
7 Further reading
8 External links
Overview[edit]
In the first part of the autobiography, Mandela describes his upbringing as a child and adolescent in South Africa, and being connected to the royal Thembu dynasty. His childhood name was Rolihlahla, which is loosely translated as "pulling the branch of a tree", or a euphemism for "troublemaker".
Mandela describes his education at a Thembu college called Clarkebury, and later at the strict Healdtown school, where students were rigorously put in routines. He mentions his education at the University of Fort Hare, and his practice of law later on. He also then writes; "Democracy meant all men to be heard, and decision was taken together as a people. Majority rule was a foreign notion. A minority was not to be clashed by a majority." (p. 29)
In the second part of the book, Mandela introduces political and social aspects of apartheid in South Africa, and the influences of politicians such as Daniel François Malan who implemented the nadir of African freedoms, as he officially commenced the apartheid policies. Mandela joined the African National Congress in 1950 and describes his organisation of guerrilla tactics and underground organisations to battle against apartheid.
In 1961, Mandela was convicted for inciting people to strike and leaving the country without a passport and sentenced to five years imprisonment. However, Mandela was shortly thereafter sentenced to life imprisonment for sabotage in what was known as the "Rivonia Trial", by Justice Dr. Quartus de Wet, instead of a possible death sentence. (p. 159)
Nelson Mandela's prison cell on Robben Island
Mandela describes prison time on Robben Island and Pollsmoor Prison. His 28-year tenure in prison was marked by the cruelty of Afrikaner guards, backbreaking labour, and sleeping in minuscule cells which were nearly uninhabitable. Unlike his biographer Anthony Sampson, Mandela does not accuse the warder James Gregory of fabricating a friendship with his prisoner. Gregory's book Goodbye Bafana discussed Mandela's family life and described Gregory as a close personal friend of Mandela. According to Mandela: The Authorised Biography, Gregory's position was to censor the letters delivered to the future president, and he thereby discovered the details of Mandela's personal life, which he then made money from by means of his book Goodbye Bafana. Mandela considered suing Gregory for this breach of trust.[3] In Long Walk to Freedom Mandela remarks of Gregory only that 'I had not known him terribly well, but he knew us, because he had been responsible for reviewing our incoming and outgoing mail.'[4]
Later on in his sentence, Mandela met South African president, Frederik Willem de Klerk, and was released from prison in 1990. Unlike his friend Anthony Sampson's account, Mandela's book does not discuss the alleged complicity of de Klerk in the violence of the eighties and nineties, or the role of his ex-wife Winnie Mandela in that bloodshed. Mandela became the South African president in 1994.
Reviews[edit]
The book won the Alan Paton Award in 1995, and has been published in numerous languages, including an Afrikaans translation by Antjie Krog.
Film adaptation[edit]
Long Walk to Freedom has been adapted into a film titled Mandela: Long Walk to Freedom directed by Justin Chadwick, written by William Nicholson, and produced by Anant Singh. Mandela personally awarded the film rights to the book to Singh's company some years before 2009. Singh believes that as the film is based on Mandela's own writing, it will be the "definitive" biopic of him.[5] English actor Idris Elba portrays Mandela in the film.[6] The film was limited released on 29 November 2013 in the United States. Full release happened on Christmas Day 2013 in the United States.[7] When the film was shown in London for Prince William and his wife, Nelson Mandela's death was announced.
Ghost writer[edit]
In an obituary of Mandela, The Times of London reported that the later chapters had been "ghosted by a skilful US journalist", and that Mandela had later started work on a second set of memoirs without a ghost writer.[8]
See also[edit]
Mandela: The Authorised Biography
"I Am Prepared to Die" speech
Apartheid
F.W. de Klerk
Arabic edition The book was translated into Arabic and published in 1998 in South Africa.
References[edit]
Jump up ^ "Long walk to freedom : the autobiography of Nelson Mandela". Franklin Record (first ed.). Philadelphia. ISBN 0316545856. OCLC 31530423. Retrieved 2017-01-21.
Jump up ^ Spencer, Clare. "The pitfalls of naming places after famous people". BBC News. 29 July 2011.
Jump up ^ Mandela: The Authorised Biography, p. 217.
Jump up ^ Nelson Mandela: Long Walk to Freedom, p. 614.
Jump up ^ Staff (13 March 2009). "Mandela's autobiography Long Walk to Freedom to be adapted into film". Xinhua News Agency. Archived from the original on 16 March 2009. Retrieved 13 March 2009.
Jump up ^ Jefferson, Lucette (22 February 2012). "Confirmed! Idris Elba set to play Nelson Mandela in Biopic". Huffington Post. Retrieved 23 February 2012.
Jump up ^ "Nelson Mandela and Saths Cooper spent Christmas in prison together". UPI.com. 12 December 2014. Retrieved 26 December 2013.
Jump up ^ "The Times Obituary: Nelson Mandela". The Times. London: Times Newspapers Ltd. 5 December 2013. Retrieved 16 February 2014.
Further reading[edit]
Sampson, Anthony (1999). Mandela: the authorised biography. HarperCollins. ISBN 0-00-638845-0.
Mandela, Nelson (1995). Long walk to freedom: the autobiography of Nelson Mandela. Little Brown & Co. ISBN 0-316-54818-9.
Brookfield, Stephen (February 2008). "Radical questioning on the Long Walk to Freedom: Nelson Mandela and the practice of critical reflection". Adult Education Quarterly. Sage for the American Association for Adult and Continuing Education (AAACE). 58 (2): 95–109. doi:10.1177/0741713607310150.
External links[edit]
Excerpts from Long Walk To Freedom
poly-lingual audio excerpts from Long Walk To Freedom (abridged edition)
Inspiring Quotes from Long Walk To Freedom
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18 July 1918 – 5 December 2013
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Columbian College of Arts and Sciences
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Columbian College
of Arts & Sciences
Motto
Deus Nobis Fiducia
(In God Our Trust)
Type
Private
Established
1821
Parent institution
George Washington University
Dean
Ben Vinson III
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1,007
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1,763
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861
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801 22nd St. NW, Washington, D.C., 20052
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Urban—Foggy Bottom
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columbian.gwu.edu
The Columbian College of Arts and Sciences (abbreviated as the Columbian College, Columbian, or CCAS) is the college of liberal arts and sciences of the George Washington University, in Washington, D.C. The Columbian College is one of the most prestigious schools of political sciences, history, English, and economics in the United States.
The Columbian College is ranked as the 7th best college of political sciences in the United States, by USA Today College rankings,[1] and is ranked in the 2018 Academic Ranking of World Universities in the top 76-100 schools of social sciences in the world.[2] CCAS is the largest school at George Washington University, with around 5,000 undergraduate students and 2,500 graduate students, and 42 academic departments, representing a significant portion of the University's instructional, scholarly and research activity.
Columbian is known for its numerous prominent alumni, particularly in the fields of government, economic development, and public policy, including numerous notable living figures, such as Anwar Gargash(current Minister of State for Foreign Affairs of the United Arab Emirates), sitting U.S. Senator Mark Warner, Vincent C. Gray (former Mayor of the District of Columbia) and Daniel Weiss (CEO of the Metropolitan Museum of Art). Historical alumni include First Lady Jacqueline Kennedy Onassis and Ralph Asher Alpher, "father of the Big Bang Theory".
Contents
1 History
2 Schools
3 Rankings
4 Undergraduate programs
5 Graduate programs
6 Notes
7 External links
History[edit]
The Old Main Building.
The Columbian College bears the original name of the George Washington University when it was chartered by the United States Congress in 1821.
The Columbian College of Arts and Sciences is the original college of the George Washington University and one of the oldest colleges in the United States. Founded as the Columbian College on February 9, 1821 by an act of Congress,[3] the college was created as a Baptist institution by Reverend Luther Rice. Originally, the college consisted of two departments: the Theological Department and Classical Department, with individual professors covering other subjects such as mathematics and anatomy.
The college's first class graduated in 1824, where the president presented each of the three graduates with their degree in the presence of the Marquis de Lafayette and college president William Staughton.[3]
With the dawn of the Civil War in 1861, the majority of the students left the college to fight for the Confederacy.
The Columbian College contains many research centers and institutes, including the Biostatistics Center.
Schools[edit]
University Yard, with Jean-Antoine Houdon's statue, George Washington.
The Columbian College of Arts and Sciences houses 42 academic departments. The Columbian College is also home to three distinct schools:
School of Media and Public Affairs (SMPA)
Corcoran School of the Arts and Design
Trachtenberg School of Public Policy and Public Administration (SPPPA)
Rankings[edit]
CCAS is ranked as the 8th best political sciences and government program in the U.S. by College Factual.[4]
U.S. News & World Report ranks CCAS's graduate programs as:
History, 59th best in the United States
Economics, 63rd best in the United States
English, 67th best in the United States
Undergraduate programs[edit]
Corcoran Hall.
Columbian College was founded in 1821 and awarded its first bachelor's degree in 1824. Today, the Columbian College offers the following baccalaureate degrees (either Bachelor of Arts or Bachelor of Science):[5]
American Studies
Anthropology
Archaeology
Art History
Fine Arts
Biochemistry
Biology
Biological Anthropology
Biophysics
Chemistry
Pre-Professional Chemistry / Pre-Med
Chinese
Classical Studies
Communication
Criminal Justice
Dance
Dramatic Literature
Early Modern European Studies
Economics
English
English and Creative Writing
Environmental Studies
Fine Arts
French
Geography
Geological Sciences
German
History
Human Services
Interior Architecture (Bachelor of Fine Arts)
Japanese
Journalism and Mass Communication
Judaic Studies
Liberal Arts
Mathematics
Music
Organizational Sciences
Peace Studies
Philosophy
Philosophy (Public Affairs)
Physics
Political Communication
Political Science
Political Science (Public Policy)
Psychology
Religion
Russian
Sociology
Spanish
Speech and Hearing Science
Statistics
Theatre
Women's, Gender, and Sexuality Studies
Graduate programs[edit]
Ten years after the Columbian College was chartered, the college conferred its first Master of Arts degree in 1831. Columbian College was also one of the first institutions in the United States to award a doctorate, as it did with a Doctor of Philosophy degree in 1888. However, the graduate program was formally established in 1905.[5]
Notes[edit]
Jump up ^ USA Today College - Best Colleges for Political Sciences
Jump up ^ ARWU - Global Social Sciences Rankings
^ Jump up to: a b "A Brief History of GW". Retrieved 2014-07-31.
Jump up ^ College Factual - Top Ranked Schools of Political Sciences and Government in the U.S.
^ Jump up to: a b "Academic Degrees". The Columbian College of Arts and Sciences. Retrieved 2009-06-20. External link in |work= (help)
External links[edit]
Wikimedia Commons has media related to Columbian College of Arts & Sciencs.
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Test-and-set
From Wikipedia, the free encyclopedia
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In computer science, the test-and-set instruction is an instruction used to write 1 (set) to a memory location and return its old value as a single atomic (i.e., non-interruptible) operation. If multiple processes may access the same memory location, and if a process is currently performing a test-and-set, no other process may begin another test-and-set until the first process's test-and-set is finished. A CPU may use a test-and-set instruction offered by another electronic component, such as dual-port RAM; a CPU itself may also offer a test-and-set instruction.
A lock can be built using an atomic test-and-set[1] instruction as follows:
function Lock(boolean *lock) {
    while (test_and_set(lock) == 1);
}

The calling process obtains the lock if the old value was 0 otherwise while-loop spins waiting to acquire the lock. This is called a spinlock. "Test and Test-and-set" is another example.
Maurice Herlihy (1991) proved that test-and-set has a finite consensus number and can solve the wait-free consensus problem for at-most two concurrent processes.[2] In contrast, compare-and-swap offers a more general solution to this problem.
Contents
[hide]
1 Hardware implementation of test-and-set
1.1 Variation 1
1.2 Variation 2
2 Software implementation of test-and-set
3 Mutual exclusion using test-and-set
3.1 pseudo-C implementation
3.2 Assembly implementation
4 Performance evaluation of test-and-set locks
5 See also
6 References
7 External links
Hardware implementation of test-and-set[edit]
DPRAM test-and-set instructions can work in many ways. Here are two variations, both of which describe a DPRAM which provides exactly 2 ports, allowing 2 separate electronic components (such as 2 CPUs) access to every memory location on the DPRAM.
Variation 1[edit]
When CPU 1 issues a test-and-set instruction, the DPRAM first makes an "internal note" of this by storing the address of the memory location in a special place. If at this point, CPU 2 happens to issue a test-and-set instruction for the same memory location, the DPRAM first checks its "internal note", recognizes the situation, and issues a BUSY interrupt, which tells CPU 2 that it must wait and retry. This is an implementation of a busy waiting or spinlock using the interrupt mechanism. Since all this happens at hardware speeds, CPU 2's wait to get out of the spin-lock is very short.
Whether or not CPU 2 was trying to access the memory location, the DPRAM performs the test given by CPU 1. If the test succeeds, the DPRAM sets the memory location to the value given by CPU 1. Then the DPRAM wipes out its "internal note" that CPU 1 was writing there. At this point, CPU 2 could issue a test-and-set, which would succeed.
Variation 2[edit]
CPU 1 issues a test-and-set instruction to write to "memory location A". The DPRAM does not immediately store the value in memory location A, but instead simultaneously moves the current value to a special register, while setting the contents of memory location A to a special "flag value". If at this point, CPU 2 issues a test-and-set to memory location A, the DPRAM detects the special flag value, and as in Variation 1, issues a BUSY interrupt.
Whether or not CPU 2 was trying to access the memory location, the DPRAM now performs CPU 1's test. If the test succeeds, the DPRAM sets memory location A to the value specified by CPU 1. If the test fails, the DPRAM copies the value back from the special register to memory location A. Either operation wipes out the special flag value. If CPU 2 now issues a test-and-set, it will succeed.
Software implementation of test-and-set[edit]
Some instruction sets have an atomic test-and-set machine language instruction - x86[3] and IBM System/360 and its successors (including z/Architecture).[4] Those that do not can still implement an atomic test-and-set using a read-modify-write or compare-and-swap instruction.
The test and set instruction when used with boolean values behaves like the following function. Crucially the entire function is executed atomically: no process can interrupt the function mid-execution and hence see a state that only exists during the execution of the function. This code only serves to help explain the behaviour of test-and-set; atomicity requires explicit hardware support and hence can't be implemented as a simple function. NOTE: In this example, 'lock' is assumed to be passed by reference (or by name) but the assignment to 'initial' creates a new value (not just copying a reference).
function TestAndSet(boolean_ref lock) {
    boolean initial = lock;
    lock = true;
    return initial;
}

The above code segment is not atomic in the sense of the test-and-set instruction. It also differs from the descriptions of DPRAM hardware test-and-set above in that here the "set" value and the test are fixed and invariant, and the "set" part of the operation is done regardless of the outcome of the test, whereas in the description of DPRAM test-and-set, the memory is set only upon passage of the test, and the value to set and the test condition are specified by the CPU. Here, the value to set can only be 1, but if 0 and 1 are considered the only valid values for the memory location, and "value is nonzero" is the only allowed test, then this equates to the case described for DPRAM hardware (or, more specifically, the DPRAM case reduces to this under these constraints). From that viewpoint, this can correctly be called "test-and-set" in the full conventional sense of the term. The essential point to note, which this software function does embody, is the general intent and principle of test-and-set: that a value both is tested and is set in one atomic operation such that no other program thread might cause the target memory location to change after it is tested but before it is set, which would violate the logic requiring that the location will only be set when it has a certain value. (That is, critically, as opposed to merely when it very recently had that value.)
In the C programming language, the implementation would be like:
 #define LOCKED 1 int TestAndSet(int* lockPtr) { int oldValue; // Start of atomic segment // The following statements should be interpreted as pseudocode for // illustrative purposes only. // Traditional compilation of this code will not guarantee atomicity, the // use of shared memory (i.e. not-cached values), protection from compiler // optimization, or other required properties. oldValue = *lockPtr; *lockPtr = LOCKED; // End of atomic segment return oldValue; }
The code also shows that TestAndSet is really two operations: an atomic read-modify-write and a test. Only the read-modify-write needs to be atomic. (This is true because delaying the value comparison itself by any amount of time will not change the result of the test, once the value to test has been obtained. Once the code writes the initial value, the result of the test has been determined, even if it has not been computed yet—e.g. in the C language example, by the == operator.)
Mutual exclusion using test-and-set[edit]
One way to implement mutual exclusion is by using a test-and-set based lock[5][6] as follows:
pseudo-C implementation[edit]
 volatile int lock = 0; void Critical() { while (TestAndSet(&lock) == 1); critical section // only one process can be in this section at a time lock = 0 // release lock when finished with the critical section }
The lock variable is a shared variable i.e. it can be accessed by all processors/threads. Note the volatile keyword. In absence of volatile, the compiler and/or the CPU(s) may optimize access to lock and/or use cached values, thus rendering the above code erroneous. Conversely, and unfortunately, the presence of volatile does not guarantee that reads and writes are committed to memory. Some compilers issue memory barriers to ensure that operations are committed to memory, but since the semantics of volatile in C/C++ is quite vague, not all compilers will do that. Consult your compiler's documentation to determine if it does.
This function can be called by multiple processes, but it is guaranteed that only one process will be in the critical section at a time. The rest of the processes will keep spinning until they get the lock. It is possible that a process is never granted the lock. In such a case it will loop endlessly. This is a drawback of this implementation as it doesn't ensure fairness. These issues are further elaborated in the performance section.
Assembly implementation[edit]
enter_region: ; A "jump to" tag; function entry point. tsl reg, flag ; Test and Set Lock; flag is the ; shared variable; it is copied ; into the register reg and flag ; then atomically set to 1. cmp reg, #0 ; Was flag zero on entry_region? jnz enter_region ; Jump to enter_region if ; reg is non-zero; i.e., ; flag was non-zero on entry. ret ; Exit; i.e., flag was zero on ; entry. If we get here, tsl ; will have set it non-zero; thus, ; we have claimed the resource ; associated with flag. leave_region: move flag, #0 ; store 0 in flag ret ; return to caller
Here tsl is an atomic instruction and flag is the lock variable. The process doesn't return unless it acquires the lock.
Performance evaluation of test-and-set locks[edit]
The four major evaluation metrics for locks in general are uncontended lock-acquisition latency, bus traffic, fairness, and storage.[7]
Test-and-set scores low on two of them, namely, high bus traffic and unfairness.
When processor P1 has obtained a lock and processor P2 is also waiting for the lock, P2 will keep incurring bus transactions in attempts to acquire the lock. When a processor has obtained a lock, all other processors which also wish to obtain the same lock keep trying to obtain the lock by initiating bus transactions repeatedly until they get hold of the lock. This increases the bus traffic requirement of test-and-set significantly. This slows down all other traffic from cache and coherence misses. It slows down the overall section, since the traffic is saturated by failed lock acquisition attempts. Test-and-test-and-set is an improvement over TSL since it does not initiate lock acquisition requests continuously.
When we consider fairness, we consider if a processor gets a fair chance of acquiring the lock when it is set free. In an extreme situation the processor might starve i.e. it might not be able to acquire the lock for an extended period of time even though it has become free during that time.
Storage overhead for TSL is next to nothing since only one lock is required. Uncontended latency is also low since only one atomic instruction and branch are needed.
See also[edit]
Fetch-and-add
Test and test-and-set
Load-link/store-conditional
Compare-and-swap
References[edit]
Jump up ^ Anderson, T. E. (1990-01-01). "The performance of spin lock alternatives for shared-money multiprocessors". IEEE Transactions on Parallel and Distributed Systems. 1 (1): 6–16. doi:10.1109/71.80120. ISSN 1045-9219.
Jump up ^ Herlihy, Maurice (January 1991). "Wait-free synchronization" (PDF). ACM Trans. Program. Lang. Syst. 13 (1): 124–149. doi:10.1145/114005.102808. Retrieved 2007-05-20.
Jump up ^ "BTS—Bit Test and Set". www.felixcloutier.com. Retrieved 2016-11-21.
Jump up ^ "IBM Knowledge Center". www.ibm.com. Retrieved 2016-11-21.
Jump up ^ Remzi H. Arpaci-Dusseau and Andrea C. Arpaci-Dusseau (2015). Operating Systems: Three Easy Pieces (0.91 ed.). Arpaci-Dusseau Books – via http://www.ostep.org/.
Jump up ^ Solihin, Yan (2009). Fundamentals of parallel computer architecture : multichip and multicore systems. p. 252. ISBN 9780984163007.
Jump up ^ Solihin, Yan (2016). Fundamentals of Parallel Architecture. Boca Raton, FL: CRC Press. ISBN 978-1-4822-1118-4.
External links[edit]
Description from Encyclopaedia of Delay-Insensitive Systems
"Wait-free Test-and-Set" by Yehuda Afek
int testandset(int *lock) - C-callable routine written in Sun SPARC assembly language
Intel Developer Manual
Retrieved from "https://en.wikipedia.org/w/index.php?title=Test-and-set&oldid=802064065"
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Angular cheilitis
From Wikipedia, the free encyclopedia
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Angular cheilitis
Synonyms
Rhagades,[1] perlèche,[2] cheilosis,[2] angular cheilosis,[2] commissural cheilitis,[2] angular stomatitis[2]
Bilateral angular cheilitis in an elderly individual with false teeth, iron deficiency anemia and dry mouth
Pronunciation
/kaɪˈlaɪtɪs/
Specialty
Dermatology
Symptoms
Redness, skin breakdown and crusting at the corner of the mouth[2]
Usual onset
Children, 30s to 60s[2]
Duration
Days to years[2]
Causes
Infection, irritation, allergies[2]
Treatment
Based on cause, barrier cream[2]
Frequency
0.7% of the population[3]
[edit on Wikidata]
Angular cheilitis (AC), is inflammation of one or both corners of the mouth.[4][5] Often the corners are red with skin breakdown and crusting.[2] It can also be itchy or painful.[2] The condition can last for days to years.[2] Angular cheilitis is a type of cheilitis (inflammation of the lips).[6]
Angular cheilitis can be caused by infection, irritation, or allergies.[2] Infections include by fungi such as Candida albicans and bacteria such as Staph. aureus.[2] Irritants include poorly fitting dentures, licking the lips or drooling, mouth breathing resulting in a dry mouth, sun exposure, overclosure of the mouth, smoking, and minor trauma.[2] Allergies may include to substances like toothpaste, makeup, and food.[2] Often a number of factors are involved.[2] Other factors may include poor nutrition or poor immune function.[2][5] Diagnosis may be helped by testing for infections and patch testing for allergies.[2]
Treatment for angular cheilitis is typically based on the underlying causes along with the use of a barrier cream.[2] Frequently an antifungal and antibacterial cream is also tried.[2] Angular cheilitis is a fairly common problem,[2] with estimates that it affects 0.7% of the population.[3] It occurs most often in the 30s to 60s, although is also relatively common in children.[2] In the developing world, iron and vitamin deficiencies are a common cause.[5]
Contents
[hide]
1 Signs and symptoms
2 Causes
2.1 Infection
2.2 Irritation contact dermatitis
2.3 Nutritional deficiencies
2.4 Systemic disorders
2.5 Drugs
2.6 Allergic contact dermatitis
3 Diagnosis
3.1 Classification
4 Management
5 Prognosis
6 Epidemiology
7 References
8 External links
Signs and symptoms[edit]
Angular cheilitis – a fissure running in the corner of the mouth with reddened, irritated facial skin adjacent.
A fairly mild case of angular cheilitis extending onto the facial skin in a young person (affected area is within the black oval).
Angular cheilitis is a fairly non specific term which describes the presence of an inflammatory lesion in a particular anatomic site (i.e. the corner of the mouth). As there are different possible causes and contributing factors from one person to the next, the appearance of the lesion is somewhat variable. The lesions are more commonly symmetrically present on both sides of the mouth,[4] but sometimes only one side may be affected. In some cases, the lesion may be confined to the mucosa of the lips, and in other cases the lesion may extend past the vermilion border (the edge where the lining on the lips becomes the skin on the face) onto the facial skin. Initially, the corners of the mouth develop a gray-white thickening and adjacent erythema (redness).[2] Later, the usual appearance is a roughly triangular area of erythema, edema (swelling) and breakdown of skin at either corner of the mouth.[2][4] The mucosa of the lip may become fissured (cracked), crusted, ulcerated or atrophied.[2][4] There is not usually any bleeding.[7] Where the skin is involved, there may be radiating rhagades (linear fissures) from the corner of the mouth. Infrequently, the dermatitis (which may resemble eczema) can extend from the corner of the mouth to the skin of the cheek or chin.[4] If Staphylococcus aureus is involved, the lesion may show golden yellow crusts.[8] In chronic angular cheilitis, there may be suppuration (pus formation), exfoliation (scaling) and formation of granulation tissue.[2][4]
Sometimes contributing factors can be readily seen, such as loss of lower face height from poorly made or worn dentures, which results in mandibular overclosure ("collapse of jaws").[9] If there is a nutritional deficiency underlying the condition, various other signs and symptoms such as glossitis (swollen tongue) may be present. In people with angular cheilitis who wear dentures, often there may be erythematous mucosa underneath the denture (normally the upper denture), an appearance consistent with denture-related stomatitis.[4] Typically the lesions give symptoms of soreness, pain, pruritus (itching) or burning or a raw feeling.[2][9]
Causes[edit]
Angular cheilitis is thought to be multifactorial disorder of infectious origin,[10] with many local and systemic predisposing factors.[11] The sores in angular cheilitis are often infected with fungi (yeasts), bacteria, or a combination thereof;[8] this may represent a secondary, opportunistic infection by these pathogens. Some studies have linked the initial onset of angular cheilitis with nutritional deficiencies, especially of the B(B2-riboflavin) vitamins and iron (which causes iron deficiency anemia),[12] which in turn may be evidence of malnutrition or malabsorption. Angular cheilitis can be a manifestation of contact dermatitis,[13] which is considered in two groups; irritational and allergic.
Infection[edit]
The involved organisms are:
Candida species alone (usually Candida albicans), which accounts for about 20% of cases,[14]
Bacterial species, either:
Staphylococcus aureus alone, which accounts for about 20% of cases,[14]
β-hemolytic streptococci alone. These types of bacteria have been detected in between 8–15% of cases of angular cheilitis,[2] but less commonly are they present in isolation,[10]
Or a combination of the above organisms, (a polymicrobial infection)[8] with about 60% of cases involving both C. albicans and S. aureus.[14][15]
Candida can be detected in 93% of angular cheilitis lesions.[2] This organism is found in the mouths of about 40% of healthy individuals, and it is considered by some to be normal commensal component of the oral microbiota.[2] However, Candida shows dimorphism, namely a yeast form which is thought to be relatively harmless and a pathogenic hyphal form which is associated with invasion of host tissues. Potassium hydroxide preparation is recommended by some to help distinguish between the harmless and the pathogenic forms, and thereby highlight which cases of angular cheilitis are truly caused by Candida.[2] The mouth may act as a reservoir of Candida that reinfects the sores at the corners of the mouth and prevents the sores from healing.
A lesion caused by recurrence of a latent herpes simplex infection can occur in the corner of the mouth. Really this is herpes labialis (a cold sore), and is sometimes termed "angular herpes simplex".[2] A cold sore at the corner of the mouth behaves similarly to elsewhere on the lips, and follows a pattern of vesicle (blister) formation followed by rupture leaving a crusted sore which resolves in about 7–10 days, and recurs in the same spot periodically, especially during periods of stress. Rather than utilizing antifungal creams, angular herpes simplex is treated in the same way as a cold sore, with topical antiviral drugs such as aciclovir.
Irritation contact dermatitis[edit]
A famous sketch by Leonardo da Vinci in preparation to depict the face of Judas Iscariot in The Last supper. The subject shows overclosure of the jaws and loss of facial support around the mouth.
Pronounced skin folds extending from the corner of the mouth.
Main article: Irritant contact dermatitis
22% of cases of angular cheilitis are due to irritants.[2] Saliva contains digestive enzymes, which may have a degree of digestive action on tissues if they are left in contact.[2] The corner of the mouth is normally exposed to saliva more than any other part of the lips. Reduced lower facial height (vertical dimension or facial support) is usually caused by edentulism (tooth loss), or wearing worn down, old dentures or ones which are not designed optimally. This results in overclosure of the mandible (collapse of the jaws),[9] which extenuates the angular skin folds at the corners of the mouth,[14] in effect creating an intertriginous skin crease. The tendency of saliva to pool in these areas is increased, constantly wetting the area,[10] which may cause tissue maceration and favors the development of a yeast infection.[14] As such, angular cheilitis is more commonly seen in edentulous people (people without any teeth).[9] It is by contrast uncommon in persons who retain their natural teeth.[16] Angular cheilitis is also commonly seen in denture wearers.[13] Angular cheilitis is present in about 30% of people with denture-related stomatitis.[10] It is thought that reduced vertical dimension of the lower face may be a contributing factor in up to 11% of elderly persons with angular cheilitis and in up to 18% of denture wearers who have angular cheilitis.[2] Reduced vertical dimension can also be caused by tooth migration, wearing orthodontic appliances, and elastic tissue damage caused by ultraviolet light exposure and smoking.[2]
Habits or conditions that keep the corners of the mouth moist might include chronic lip licking, thumb sucking (or sucking on other objects such as pens, pipes, lollipops), dental cleaning (e.g. flossing), chewing gum, hypersalivation, drooling and mouth breathing.[2][4][14] Some consider habitual lip licking or picking to be a form of nervous tic, and do not consider this to be true angular cheilitis,[4] instead calling it perlèche (derived from the French word pourlècher meaning "to lick one’s lips"),[2] or "factitious cheilitis" is applied to this habit.[2] The term "cheilocandidiasis" describes exfoliative (flaking) lesions of the lips and the skin around the lips, and is caused by a superficial candidal infection due to chronic lip licking.[14] Less severe cases occur during cold, dry weather, and is a form of chapped lips. Individuals may lick their lips in an attempt to provide a temporary moment of relief, only serving to worsen the condition.[17]
The sunscreen in some types of lip balm degrades over time into an irritant. Using expired lipbalm can initiate mild angular cheilitis, and when the person applies more lipbalm to alleviate the cracking, it only aggravates it. Because of the delayed onset of contact dermatitis and the recovery period lasting days to weeks, people typically do not make the connection between the causative agent and the symptoms.[medical citation needed]
Nutritional deficiencies[edit]
Several different nutritional deficiency states of vitamins or minerals have been linked to AC.[5] It is thought that in about 25% of people with AC, iron deficiency or deficiency of B vitamins are involved.[5] Nutritional deficiencies may be a more common cause of AC in Third World countries.[5] Chronic iron deficiency may also cause koilonychia (spoon shaped deformity of the fingernails) and glossitis (inflammation of the tongue). It is not completely understood how iron deficiency causes AC, but it is known that it causes a degree of immunocompromise (decreased efficiency of the immune system) which may in turn allow an opportunistic infection of candida.[5] Vitamin B2 deficiency (ariboflavinosis) may also cause AC, and other conditions such as redness of mucous membranes, magenta colored glossitis (pink inflammation of the tongue).[5] Vitamin B5 deficiency may also cause AC, along with glossitis, and skin changes similar to seborrhoeic dermatitis around the eyes, nose and mouth.[5] Vitamin B12 deficiency is sometimes responsible for AC, and commonly occurs together with folate deficiency (a lack of folic acid), which also causes glossitis and megaloblastic anemia.[5] Vitamin B3 deficiency (pellagra) is another possible cause, and in which other association conditions such as dermatitis, diarrhea, dementia and glossitis can occur.[5] Biotin (vitamin B7) deficiency has also been reported to cause AC, along with hair loss (alopecia) and dry eyes.[5] Zinc deficiency is known to cause AC.[18] Other symptoms may include diarrhea, alopecia and dermatitis.[5] Acrodermatitis enteropathica is an autosomal recessive genetic disorder causing impaired absorption of zinc, and is associated with AC.[5]
In general, these nutritional disorders may be caused by malnutrition, such as may occur in alcoholism or in poorly considered diets, or by malabsorption secondary to gastrointestinal disorders (e.g. Coeliac disease or chronic pancreatitis) or gastrointestinal surgeries (e.g. pernicious anemia caused by ileal resection in Crohn's disease).[5]
Systemic disorders[edit]
Some systemic disorders are involved in angular cheilitis by virtue of their association with malabsorption and the creation of nutritional deficiencies described above. Such examples include people with anorexia nervosa.[5] Other disorders may cause lip enlargement (e.g. orofacial granulomatosis),[5] which alters the local anatomy and extenuates the skin folds at the corners of the mouth. More still may be involved because they affect the immune system, allowing normally harmless organisms like Candida to become pathogenic and cause an infection. Xerostomia (dry mouth) is thought to account for about 5% of cases of AC.[5] Xerostomia itself has many possible causes, but commonly the cause may be side effects of medications, or conditions such as Sjögren's syndrome. Conversely, conditions which cause drooling or sialorrhoea (excessive salivation) can cause angular cheilitis by creating a constant wet environment in the corners of the mouth. About 25% of people with Down syndrome appear to have AC.[5] This is due to relative macroglossia, an apparently large tongue in a small mouth, which may constantly stick out of the mouth causing maceration of the corners of the mouth with saliva. Inflammatory bowel diseases (such as Crohn's disease or ulcerative colitis) can be associated with angular cheilitis.[4] In Crohn's, it is likely the result of malabsorption and immunosuppressive therapy which gives rise to the sores at the corner of the mouth.[9] Glucagonomas are rare pancreatic endocrine tumors which secrete glucagon, and cause a syndrome of dermatitis, glucose intolerance, weight loss and anemia. AC is a common feature of glucagonoma syndrome.[19] Infrequently, angular cheilitis may be one of the manifestations of chronic mucocutaneous candidiasis,[14] and sometimes cases of oropharyngeal or esophageal candidiasis may accompany angular cheilitis.[2] Angular cheilitis may be present in human immunodeficiency virus infection,[11] neutropenia,[16] or diabetes.[4] Angular cheilitis is more common in people with eczema because their skin is more sensitive to irritants.[2] Other conditions possibly associated include plasma cell gingivitis,[7] Melkersson-Rosenthal syndrome,[5] or sideropenic dysphagia (also called Plummer-Vinson syndrome or Paterson-Brown-Kelly syndrome).[5]
Drugs[edit]
Several drugs may cause AC as a side effect, by various mechanisms, such as creating drug-induced xerostomia. Various examples include isotretinoin, indinavir, and sorafenib.[5] Isotretinoin (Accutane), an analog of vitamin A, is a medication which dries the skin. Less commonly, angular cheilitis is associated with primary hypervitaminosis A,[20] which can occur when large amounts of liver (including cod liver oil and other fish oils) are regularly consumed or as a result from an excess intake of vitamin A in the form of vitamin supplements. Recreational drug users may develop AC. Examples include cocaine, methamphetamines, heroin, and hallucinogens.[5]
Allergic contact dermatitis[edit]
See also: Allergic contact cheilitis, Allergic contact dermatitis, and Allergic contact stomatitis
Patch test
Allergic reactions may account for about 25–34% of cases of generalized cheilitis (i.e., inflammation not confined to the angles of the mouth). It is unknown how frequently allergic reactions are responsible for cases of angular cheilitis, but any substance capable of causing generalized allergic cheilitis may present involving the corners of the mouth alone.
Examples of potential allergens include substances that may be present in some types of lipstick, toothpaste, acne products, cosmetics, chewing gum, mouthwash, foods, dental appliances, and materials from dentures or mercury containing amalgam fillings.[2] It is usually impossible to tell the difference between irritant contact dermatitis and allergic contact dermatitis without a patch test.
Diagnosis[edit]
Photographic Comparison of: 1) a Canker Sore - inside the mouth, 2) Herpes, 3) Angular Cheilitis and 4) Chapped Lips.
Angular chielitis is normally a diagnosis made clinically. If the sore is unilateral, rather than bilateral, this suggests a local factor (e.g., trauma) or a split syphilitic papule.[4][21] Angular cheilitis caused by mandibular overclosure, drooling, and other irritants is usually bilateral.[2]
The lesions are normally swabbed to detect if Candida or pathogenic bacterial species may be present. Persons with angular cheilitis who wear dentures often also will have their denture swabbed in addition. A complete blood count (full blood count) may be indicated, including assessment of the levels of iron, ferritin, vitamin B12 (and possibly other B vitamins), and folate.[4]
Classification[edit]
Angular cheilitis could be considered to be a type of cheilitis or stomatitis. Where Candida species are involved, angular cheilitis is classed as a type of oral candidiasis, specifically a primary (group I) Candida-associated lesion.[11] This form angular cheilitis which is caused by Candida is sometimes termed "Candida-associated angular cheilitis",[11] or less commonly, "monilial perlèche".[2] Angular cheilitis can also be classified as acute (sudden, short-lived appearance of the condition) or chronic (lasts a long time or keeps returning), or refractory (the condition persists despite attempts to treat it).[2]
Management[edit]
Angular cheilitis being treated with crystal violet tincture
There are 4 aspects to the treatment of angular cheilitis.[22] Firstly, potential reservoirs of infection inside the mouth are identified and treated.[22] Oral candidiasis, especially denture-related stomatitis is often found to be present where there is angular cheilitis, and if it is not treated, the sores at the corners of the mouth may often recur.[8][13] This involves having dentures properly fitted and disinfected. Commercial preparations are marketed for this purpose, although dentures may be left in dilute (1:10 concentration) household bleach overnight, but only if they are entirely plastic and do not contain any metal parts, and with rinsing under clean water before use.[9] Improved denture hygiene is often required thereafter, including not wearing the denture during sleep and cleaning it daily.[4] For more information, see Denture-related stomatitis.
Secondly, there may be a need to increase the vertical dimension of the lower face to prevent overclosure of the mouth and formation of deep skin folds.[22] This may require the construction of a new denture with an adjusted bite.[4] Rarely, in cases resistant to normal treatments, surgical procedures such as collagen injections (or other facial fillers such as autologous fat or crosslinked hyaluronic acid) are used in an attempt to restore the normal facial contour.[2][4] Other measures which seek to reverse the local factors that may be contributing to the condition include improving oral hygiene, stopping smoking or other tobacco habits and use of a barrier cream (e.g. zinc oxide paste) at night.[2]
Thirdly, treatment of the infection and inflammation of the lesions themselves is addressed. This is usually with topical antifungal medication,[8] such as clotrimazole,[14] amphotericin B,[22] ketoconazole,[16] or nystatin cream.[9] Some antifungal creams are combined with corticosteroids such as hydrocortisone[8] or triamcinolone[9] to reduce inflammation, and certain antifungals such as miconazole also have some antibacterial action.[8] Diiodohydroxyquinoline is another topical therapy for angular cheilitis.[14] If Staphylococcus aureus infection is demonstrated by microbiological culture to be responsible (or suspected), the treatment may be changed to fusidic acid cream,[8] an antibiotic which is effective against this type of bacteria. Aside from fusidic acid, neomycin,[22] mupirocin,[2] metronidazole,[7] and chlorhexidine[22] are alternative options in this scenario.
Finally, if the condition appears resistant to treatment, investigations for underlying causes such as anemia or nutrient deficiencies or HIV infection.[22] Identification of the underlying cause is essential for treating chronic cases. The lesions may resolve when the underlying disease is treated, e.g. with a course of oral iron or B vitamin supplements.[4] Patch testing is recommended by some in cases which are resistant to treatment and where allergic contact dermatitis is suspected.[2]
Prognosis[edit]
Most cases of angular cheilitis respond quickly when antifungal treatment is used.[16] In more long standing cases, the severity of the condition often follows a relapsing and remitting course over time.[14] The condition can be difficult to treat and can be prolonged.[4]
Epidemiology[edit]
AC is a relatively common condition,[11] accounting for between 0.7 – 3.8% of oral mucosal lesions in adults and between 0.2 – 15.1% in children, though overall it occurs most commonly in adults in the third to sixth decades of life.[2][4] It occurs worldwide, and both males and females are affected.[4] Angular cheilitis is the most common presentation of fungal and bacterial infections of the lips.[14]
References[edit]
Jump up ^ Pindborg, Jens Jørgen (1973). Atlas of Diseases of the Oral Mucosa. Saunders. ISBN 9780721672649. Archived from the original on 10 September 2017. Retrieved 17 September 2014. Angular cheilosis: The lateral lip fissures, well known among denture wearers, have been called by a variety of names, such as "rhagades", "perleche", "angular cheilitis", and "angular cheilosis".
^ Jump up to: a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az Park, KK; Brodell, RT; Helms, SE (June 2011). "Angular cheilitis, part 1: local etiologies". Cutis. 87 (6): 289–95. PMID 21838086.
^ Jump up to: a b Lyons, Faye (2014). Dermatology for the Advanced Practice Nurse. Springer Publishing Company. p. 95. ISBN 9780826136442. Archived from the original on 2016-08-16.
^ Jump up to: a b c d e f g h i j k l m n o p q r s t Scully, Crispian (2008). Oral and maxillofacial medicine : the basis of diagnosis and treatment (2nd ed.). Edinburgh: Churchill Livingstone. pp. 147–49. ISBN 9780443068188.
^ Jump up to: a b c d e f g h i j k l m n o p q r s t u v w Park, KK; Brodell RT; Helms SE. (July 2011). "Angular cheilitis, part 2: nutritional, systemic, and drug-related causes and treatment" (PDF). Cutis. 88 (1): 27–32. PMID 21877503. Archived from the original (PDF) on 2014-04-19.
Jump up ^ Martin, Elizabeth (2015). Concise Medical Dictionary. Oxford University Press. p. 136. ISBN 9780199687817. Archived from the original on 2016-08-16.
^ Jump up to: a b c Wood, NK; Goaz, PW (1997). Differential diagnosis of oral and maxillofacial lesions (5th ed.). St. Louis [u.a.]: Mosby. pp. 64–65, 85. ISBN 978-0815194323.
^ Jump up to: a b c d e f g h Coulthard P, Horner K, Sloan P, Theaker E (2008). Master dentistry volume 1, oral and maxillofacial surgery, radiology, pathology and oral medicine (2nd ed.). Edinburgh: Churchill Livingstone/Elsevier. pp. 180–81. ISBN 9780443068966.
^ Jump up to: a b c d e f g h Treister NS, Bruch JM (2010). Clinical oral medicine and pathology. New York: Humana Press. pp. 92–93, 144. ISBN 978-1-60327-519-4.
^ Jump up to: a b c d Soames JV, Southam JC, JV (1999). Oral pathology (3rd ed.). Oxford: Oxford Univ. Press. pp. 197–98. ISBN 0192628941.
^ Jump up to: a b c d e Tyldesley WR, Field A, Longman L (2003). Tyldesley's Oral medicine (5th ed.). Oxford: Oxford University Press. pp. 37, 40, 46, 63–67. ISBN 0192631470.
Jump up ^ MedlinePlus (2005-08-01). "Riboflavin (vitamin B2) deficiency (ariboflavinosis)". National Institutes of Health. Archived from the original on 2010-07-24.
^ Jump up to: a b c Peter C. Schalock, M.D.; Jeffrey T. S. Hsu, M.D.; Kenneth A. Arndt (eds.). Primary Care Dermatology. Lippincott Williams & Wilkins, 2010. p. 265. ISBN 978-0-7817-9378-0. Archived from the original on 2017-09-10.
^ Jump up to: a b c d e f g h i j k l Neville BW, Damm DD, Allen CA, Bouquot JE (2002). Oral & maxillofacial pathology (2nd ed.). Philadelphia: W.B. Saunders. pp. 100, 192, 196, 266. ISBN 0721690033.
Jump up ^ Kerawala C; Newlands C, eds. (2010). Oral and maxillofacial surgery. Oxford: Oxford University Press. p. 446. ISBN 9780199204830.
^ Jump up to: a b c d Greenberg MS, Glick M (2003). Burket's oral medicine diagnosis & treatment (10th ed.). Hamilton, Ont.: BC Decker. pp. 97–98, 550. ISBN 1550091867.
Jump up ^ Gibson, Lawrence E., M.D., "Dry Skin" Archived 2009-09-15 at the Wayback Machine., Mayo Clinic
Jump up ^ Gaveau D, Piette F, Cortot A, Dumur V, Bergoend H (1987). "[Cutaneous manifestations of zinc deficiency in ethylic cirrhosis].". Ann Dermatol Venereol. 114 (1): 39–53. PMID 3579131.
Jump up ^ Tadataka Yamada; David Alpers; Anthony Kalloo; Neil Kaplowitz; Chung Owyang; Don Powell, eds. (2009). Textbook of gastroenterology (5th ed.). Chichester, West Sussex: Blackwell Pub. pp. 1882–83. ISBN 978-1-4051-6911-0.
Jump up ^ Kliegman: Nelson Textbook of Pediatrics, 18th ed.
Jump up ^ Leyse-Wallace, Ruth (29 January 2013). Nutrition and Mental Health. CRC Press. p. 246. ISBN 9781439863350. Archived from the original on 10 September 2017. Retrieved 17 September 2014.
^ Jump up to: a b c d e f g Samaranayake, LP (2009). Essential microbiology for dentistry (3rd ed.). Elseveier. pp. 296–97. ISBN 978-0702041679.
External links[edit]
Classification
V · T · D
ICD-10: K13.0
ICD-9-CM: 528.5, 686.8
MeSH: D002613

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Microdontia
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Premature eruption
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Edentulism
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[show]
Periodontium (gingiva, periodontal ligament, cementum, alveolus) – Gums and tooth-supporting structures
Cementicle
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Gigantiform
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Epulis
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Gingival cyst of the newborn
Gingivitis
Desquamative
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Aggressive
As a manifestation of systemic disease
Chronic
Perio-endo lesion
Teething
[show]
Periapaical, mandibular and maxillary hard tissues – Bones of jaws
Agnathia
Alveolar osteitis
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Microgenia
Micrognathia
Intraosseous cysts
Odontogenic: periapical
Dentigerous
Buccal bifurcation
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Non-odontogenic: Nasopalatine duct
Median mandibular
Median palatal
Traumatic bone
Osteoma
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Osteonecrosis
Bisphosphonate-associated
Neuralgia-inducing cavitational osteonecrosis
Osteoradionecrosis
Osteoporotic bone marrow defect
Paget's disease of bone
Periapical abscess
Phoenix abscess
Periapical periodontitis
Stafne defect
Torus mandibularis
[show]
Temporomandibular joints, muscles of mastication and malocclusions – Jaw joints, chewing muscles and bite abnormalities
Bruxism
Condylar resorption
Mandibular dislocation
Malocclusion
Crossbite
Open bite
Overbite
Overeruption
Overjet
Prognathia
Retrognathia
Scissor bite
Maxillary hypoplasia
Temporomandibular joint dysfunction
[show]
Salivary glands
Benign lymphoepithelial lesion
Ectopic salivary gland tissue
Frey's syndrome
HIV salivary gland disease
Necrotizing sialometaplasia
Mucocele
Ranula
Pneumoparotitis
Salivary duct stricture
Salivary gland aplasia
Salivary gland atresia
Salivary gland diverticulum
Salivary gland fistula
Salivary gland hyperplasia
Salivary gland hypoplasia
Salivary gland neoplasms
Benign: Basal cell adenoma
Canalicular adenoma
Ductal papilloma
Monomorphic adenoma
Myoepithelioma
Oncocytoma
Papillary cystadenoma lymphomatosum
Pleomorphic adenoma
Sebaceous adenoma
Malignant: Acinic cell carcinoma
Adenocarcinoma
Adenoid cystic carcinoma
Carcinoma ex pleomorphic adenoma
Lymphoma
Mucoepidermoid carcinoma
Sclerosing polycystic adenosis
Sialadenitis
Parotitis
Chronic sclerosing sialadenitis
Sialectasis
Sialocele
Sialodochitis
Sialosis
Sialolithiasis
Sjögren's syndrome
[show]
Orofacial soft tissues – Soft tissues around the mouth
Actinomycosis
Angioedema
Basal cell carcinoma
Cutaneous sinus of dental origin
Cystic hygroma
Gnathophyma
Ludwig's angina
Macrostomia
Melkersson–Rosenthal syndrome
Microstomia
Noma
Oral Crohn's disease
Orofacial granulomatosis
Perioral dermatitis
Pyostomatitis vegetans
[show]
Other
Eagle syndrome
Hemifacial hypertrophy
Facial hemiatrophy
Oral manifestations of systemic disease
Salivary microbiome
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