Sandbox:Zoon balanitis: Difference between revisions

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==== Histopathology ====
==== Histopathology ====
ZB has distinctive histopathological features, which include:
ZB has distinctive histopathological features, which include:<ref name="pmid124545962">{{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>


==== Epidermal ====
==== 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
Epidermal changes include, early thickening, acanthosis and parakeratosis of epidermis, which is followed by atrophy, erosions and spongiosis.  


Early changes
Scattered neutrophils can be present in superficial erosions of the epidermis.


thickening, acanthosis, and parakeratosis, which is followed by followed by epidermal atrophy.
Spongiosis accentuation occurs in the lower half of the spinous zone.  


epidermal atrophy, can be associated with erosions and spongiosis.
Subepidermal clefts, necrotic keratinocytes, and lozenge keratinocytes can be seen in the late stages of ZB.
 
Additional features include:
 
subepidermal clefts
 
necrotic keratinocytes,
 
lozenge keratinocytes


==== Dermal ====
==== Dermal ====
ZB has very distinct histopathological changes affecting both epidermis and dermis.[13]
Dermal changes include  patchy lichenoid infiltrate of lymphocytes and plasma cells in papillary dermis, which are replaced by plasma cells, neutrophils, eosinophils, lymphocytes, and erythrocytes.  
 
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.


Dermal  vascular dilatation with singular vertical or oblique orientation of proliferated individual vessels, is a characteristic feature  of ZB.


==Epidemiology and Demographics==
In the later stages, upper dermis shows fibrosis which correlates well with subepidermal clefts, epidermal atrophy, and plasma cell infiltrates.


== Epidemiology and Demographics ==


==Screening==
==Screening==

Revision as of 19:26, 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:[8]

Epidermal

Epidermal changes include, early thickening, acanthosis and parakeratosis of epidermis, which is followed by atrophy, erosions and spongiosis.

Scattered neutrophils can be present in superficial erosions of the epidermis.

Spongiosis accentuation occurs in the lower half of the spinous zone.

Subepidermal clefts, necrotic keratinocytes, and lozenge keratinocytes can be seen in the late stages of ZB.

Dermal

Dermal changes include patchy lichenoid infiltrate of lymphocytes and plasma cells in papillary dermis, which are replaced by plasma cells, neutrophils, eosinophils, lymphocytes, and erythrocytes.

Dermal vascular dilatation with singular vertical or oblique orientation of proliferated individual vessels, is a characteristic feature of ZB.

In the later stages, upper dermis shows fibrosis which correlates well with subepidermal clefts, epidermal atrophy, and plasma cell infiltrates.

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.
  8. ↑ 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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