Sandbox:Zoon balanitis: Difference between revisions

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===Pathogenesis===
===Pathogenesis===
The exact pathogenesis is not clearly known, but following theories have been postulated:<ref name="pmid11319970">{{cite journal| author=Porter WM, Bunker CB| title=The dysfunctional foreskin. | journal=Int J STD AIDS | year= 2001 | volume= 12 | issue= 4 | pages= 216-20 | pmid=11319970 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11319970  }}</ref>
* Accumlation of epithelial debris and secretions between foreskin and penis proximal to coronal sulcus, smegma,  poor genital hygiene, repeated local infections, hot and humid weather results in chronic physical irritation or subclinical trauma, which in turn results in skin lesion along the lines of the trauma.
* Chronic infection with ''Mycobacterium smegmatis'' and human papillomaviruses (HPV) was found to be associated with development of Zoon balanitis.<ref name="pmid15588560">{{cite journal| author=Pastar Z, Rados J, Lipozencić J, Skerlev M, Loncarić D| title=Zoon plasma cell balanitis: an overview and role of histopathology. | journal=Acta Dermatovenerol Croat | year= 2004 | volume= 12 | issue= 4 | pages= 268-73 | pmid=15588560 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15588560  }}</ref>
* Many theories, which include 1) local disturbance of circulation, 2) hypersensitivity response mediated by IgE class of antibodies, 3) “extramedullary plasmacytic infiltrations that persists are expressions of occult multiple myeloma” have been postulated, no supportive evidence have been found for these hypothesis.<ref name="pmid12454596">{{cite journal| author=Weyers W, Ende Y, Schalla W, Diaz-Cascajo C| title=Balanitis of Zoon: a clinicopathologic study of 45 cases. | journal=Am J Dermatopathol | year= 2002 | volume= 24 | issue= 6 | pages= 459-67 | pmid=12454596 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12454596  }}</ref>


Etiology and pathogenesis of this condition are still speculative. As it is mostly seen in uncircumcised men, it is thought to be because of irritation, due to retention of urine and smegma in context of “dysfunctional prepuce,” leading to poor genital hygiene and repeated local infection.[9] In addition, trauma, friction, heat, and constant rubbing may be a contributory factors.[9] Thus, the two most important triggering factors are the constant exposure of the mucosa to humid condition and to chronic irritation.[10] This explains why lesions of ZB undergo prolonged remission after circumcision.[10]
==== Histopathology ====
ZB has distinctive histopathological features, which include:


In addition, other possible causes of ZB that have been described in the literature include chronic infection with ''Mycobacterium smegmatis'' and human papillomaviruses (HPV).[11] However, no evidence has yet been reported for bacterial infection and polymerase chain reaction has also failed to detect DNA of HPV.[12] Similarly, there is no evidence for the supposition that ZB may be caused by local disturbance of circulation.[13] It has also been related to lichen aureus due to marked hemorrhage in association with lichenoid infiltrate that is seen in ZB.[14] However, lichen aureus usually affects the lower limbs and is not associated with common histopathological signs of ZB such as erosions, neutrophils, and plasma cells. Thus, there is a lack of supportive evidence for this hypothesis.[13] Furthermore, there is no supportive evidence for the hypothesis given by Nishimura ''et al''.,[15] who had suggested that immediate hypersensitivity response mediated by IgE class of antibodies plays an important role in the etiopathogenesis of ZB. Hyman and Leider speculated that “extramedullary plasmacytic infiltrations that persists are expressions of occult multiple myeloma” and could be a cause ZB.[16] However, it has been contradicted by subsequent studies that have demonstrated clearly the polyclonal nature of the plasmacytic infiltration in ZB.[13]
==== Epidermal ====
Epidermal changes include, early thickening, acanthosis and parakeratosis of epidermis, which is followed by atrophy, erosions and spongiosis. Scatth eutrophils can be present in super


==== Histopathology ====
Early changes
 
thickening, acanthosis, and parakeratosis, which is followed by followed by epidermal atrophy.
 
epidermal atrophy, can be associated with erosions and spongiosis.
 
Additional features include:
 
subepidermal clefts
 
necrotic keratinocytes,
 
lozenge keratinocytes
 
==== Dermal ====
ZB has very distinct histopathological changes affecting both epidermis and dermis.[13]
ZB has very distinct histopathological changes affecting both epidermis and dermis.[13]


Revision as of 16:11, 19 January 2017

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Vishal Devarkonda, M.B.B.S[2]

Synonyms and keywords:Balanoposthite chronique circonscrite bénigne á plasmocytes, Balanitis chronica circumscripta plasmacellularis

Overview

Zoon's balanitis is an idiopathic, chronic, benign inflammatory mucositis of the genitalia.

Historical Perspective

  • In 1952, for the first time in medical literature, Zoon recognized a distinct entity in patients with chronic balanitis, named it as balanoposthite chronique circonscrite bénigne á plasmocytes” or “balanitis chronica circumscripta plasmacellularis.[1]
  • In 1954, Garnier reported the similar lesion in vulva.[2]
  • In 1956, Nikolowski described the identical lesion in oral mucosa.[3]
  • In 1963, Kortnig described the idential lesion in conjuntiva.[4]

Classification

There is no established classification system for Zoon balanitis.

Pathophysiology

Pathogenesis

The exact pathogenesis is not clearly known, but following theories have been postulated:[5]

  • Accumlation of epithelial debris and secretions between foreskin and penis proximal to coronal sulcus, smegma, poor genital hygiene, repeated local infections, hot and humid weather results in chronic physical irritation or subclinical trauma, which in turn results in skin lesion along the lines of the trauma.
  • Chronic infection with Mycobacterium smegmatis and human papillomaviruses (HPV) was found to be associated with development of Zoon balanitis.[6]
  • Many theories, which include 1) local disturbance of circulation, 2) hypersensitivity response mediated by IgE class of antibodies, 3) “extramedullary plasmacytic infiltrations that persists are expressions of occult multiple myeloma” have been postulated, no supportive evidence have been found for these hypothesis.[7]

Histopathology

ZB has distinctive histopathological features, which include:

Epidermal

Epidermal changes include, early thickening, acanthosis and parakeratosis of epidermis, which is followed by atrophy, erosions and spongiosis. Scatth eutrophils can be present in super

Early changes

thickening, acanthosis, and parakeratosis, which is followed by followed by epidermal atrophy.

epidermal atrophy, can be associated with erosions and spongiosis.

Additional features include:

subepidermal clefts

necrotic keratinocytes,

lozenge keratinocytes

Dermal

ZB has very distinct histopathological changes affecting both epidermis and dermis.[13]

Epidermal changes → Earliest histopathological changes show epidermal thickening, acanthosis, and parakeratosis. This is followed by epidermal atrophy, at times erosions and spongiosis. These superficial erosions can be associated with scattered neutrophils in the upper reaches of epidermis. Accentuation of spongiosis occurs in the lower half of the spinous zone. Additional features such as subepidermal clefts, necrotic keratinocytes, and lozenge keratinocytes (i.e., elongated keratinocytes in the lower half of the spinous zone arranged parallel to the skin surface) may be seen in the later stages of ZB.

Dermal changes → Initially, there is a patchy lichenoid infiltrate of lymphocytes and some plasma cells in papillary dermis, which is subsequently replaced by dense band-like infiltrate of plasma cells, neutrophils, eosinophils, lymphocytes, and erythrocytes. Among all these infiltrate, plasmocytes are predominant usually exceeding 50% of all the cells. It may be associated with siderophages (i.e., macrophage that has absorbed iron-containing particles), hemosiderin deposition and extravasated red blood cells. Changes in dermal vasculature include vascular dilatation with singular vertical or oblique orientation of proliferated individual vessels, which is characteristic of ZB. These are more common in cases with a dense infiltrate. In the later stages, upper dermis shows fibrosis which correlates well with subepidermal clefts, epidermal atrophy, and plasma cell infiltrates. Immunohistochemical studies of plasmocytes in ZB show that plasmocytes produce immunoglobulin G (IgG) predominantly to a lesser degree IgA and IgM.[10]

It is relatively simple to differentiate the premalignant lesions from ZB histopathologically as one can see dysplastic epithelium in the premalignant lesions while it is absent in case of ZB. Histologically, benign conditions such as pemphigus vulgaris, flexural psoriasis, lichen planus, and Reiter's disease may show features in common with ZB but lack the typical changes in the epidermis and dermal blood vessels.


Epidemiology and Demographics

Screening

There is no established screening guidelines for Zoon balanitis

Natural History, Complications, and Prognosis

Natural history

Complications

Prognosis

Diagnosis

History and symptoms

Physical examination

Laboratory findings

Treatment

Medical Therapy

Prevention

Primary Prevention

Secondary prevention

References

  1. ↑ ZOON JJ (1952). "[Chronic benign circumscript plasmocytic balanoposthitis]". Dermatologica. 105 (1): 1–7. PMID 12979576.
  2. ↑ Sonnex TS, Dawber RP, Ryan TJ, Ralfs IG (1982). "Zoon's (plasma-cell) balanitis: treatment by circumcision". Br J Dermatol. 106 (5): 585–8. PMID 7073984.
  3. ↑ NIKOLOWSKI W, WIEHL R (1956). "[Not Available]". Arch Klin Exp Dermatol. 202 (4): 347–57. PMID 13340789.
  4. ↑ KORTING GW, THEISEN H (1963). "[CIRCUMSCRIBED PLASMA CELL BALANOPOSTHITIS AND CONJUNCTIVITIS IN THE SAME PATIENT]". Arch Klin Exp Dermatol. 217: 495–504. PMID 14098119.
  5. ↑ Porter WM, Bunker CB (2001). "The dysfunctional foreskin". Int J STD AIDS. 12 (4): 216–20. PMID 11319970.
  6. ↑ Pastar Z, Rados J, Lipozencić J, Skerlev M, Loncarić D (2004). "Zoon plasma cell balanitis: an overview and role of histopathology". Acta Dermatovenerol Croat. 12 (4): 268–73. PMID 15588560.
  7. ↑ Weyers W, Ende Y, Schalla W, Diaz-Cascajo C (2002). "Balanitis of Zoon: a clinicopathologic study of 45 cases". Am J Dermatopathol. 24 (6): 459–67. PMID 12454596.

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