**2. Historical overview**

Ferdinand Ritter von Hebra (1816-1880), famed dermatologist and co-founder of the renowned Vienna School of Dermatology, is credited with the first scientific description of the skin disease, he termed leichen ruber planus (in 1860). [4] But it was the famed British Dermatologist, Erasmus Wilson (1809-1884), who originally used the term lichen planus in his publication in 1869, noting the disorder in a group of 50 patients. [5] Lichen planus obtained its name because of the lacy white lines that bear a close resemblance to the symbiont, lichen, a composite organism consisting of a fungus (the mycobiont) and a photosynthetic partner (the photobiont or phycobiont, usually, a green algae) living together in a symbiotic relationship, seen growing on rocks (Figure 1). However, Ferdinand Ritter von Hebra used the term "lichen" to denote skin lesions which are exclusively nodular, that is characterised by a macular-papular skin eruption, hence, terms such as lichen pilaris (better known as Keratosis pilaris), and lichen nitidus are still used for other skin diseas‐ es, whose appearance differs markedly from that of lichen planus. [4] Heinrich Köbner (1838–1904) described the phenomenon that bears his name in 1872, at a meeting of the Silesian Society for National Culture. Four years later (1876) he published a paper describ‐ ing his original patient describing the development of isomorphic pathologic lesions in response to trauma in previously uninvolved sites of patients with skin diseases, most often seen in patients with psoriasis, but also in eczema and lichen planus. [6] These new lesions are clinically and histopathologically identical to those in the diseased skin and/or muco‐ sa. Louis Frédéric Wickham (1861-1913) is acknowledged as the first to describe the characteristic, fine, white or grey lines known as Wickham's striae (striae is derived from Latin for groove) or dots seen on the top of the pruritic papular rash of lichen planus of the skin, and also seen with OLP. [7] In 1910 François Henri Hallopeau reported the first case of OLP-related oral carcinoma. [8]

**2.1. Epidemiology**

**2.2. Pathogenesis**

synergistic:

**5.** genetic factors.

dominated by cytotoxic CD8+

remain unknown and elusive.

**1.** antigen-specific cell-mediated immune response

**3. Antigen-specific cell-mediated immune response**

followed by (3) induction of basal keratinocyte apoptosis. [12]

and the promotion of autoimmunity

**3.** role of the humoral immune response

**4.** non-specific immune mechanisms; and

OLP is a common condition, with a prevalence of between 0.5-2.2% of the population. [1, 9] However, a recent review of epidemiological studies specific to OLP, found only one study as being the most useful, being the most free of error and bias and so, is regarded as the most reliable estimation of population prevalence of OLP, at least in European populations with a reported prevalence of 1.27%. [10, 11] However, OLP most frequently presents in women, aged 40 years and above, by a ratio of approximately 3:1 to 3:2 compared with men, of the same age.

The oral mucosa appears to have a limited immunological repertoire, predominantly a lichenoid-type reaction. This is characterised by delayed-type IV hypersensitivity reaction,

being the final common immunopathological pathway due to variety of insults, such as the development of autoantibodies against self-antigens, interaction with allergens, such as various drugs or dental materials, viruses, namely Hepatitis C (HCV), trauma (mechanical and chemical) and even stress. [12] However, the specifics, including the precise triggering factors,

The mechanisms involved in the aetio-pathogenesis of OLP are multifactorial and likely to be

**2.** loss of tolerance evidenced by the development of autoantibodies against self-antigens

The antigen that serves as the trigger and/or driver of the immune responses seen in OLP is unknown. It is likely, in the majority of cases, to be an endogenous peptide, a protein sequence innate to the basal keratinocyte; therefore, OLP can be characterised as an auto-immune condition. It is also likely that supposed exogenous triggers for OLP, such as dental materials, certain drugs, viruses and even trauma serve to expose such self-antigens, or, alter the normal innate peptide sequences so that they are perceived by the immune-surveillance cells and system as being "non-self, that is "foreign". The immune responses to this, as yet, unidentified antigen develops in three stages: (1) T-cell migration into the epithelium, (2) T-cell activation,

T-lymphocyte induced apoptosis of the basal keratinocytes,

Oral Lichen Planus

151

http://dx.doi.org/10.5772/56482

**Figure 1.** Foliose lichens growing on rock

### **2.1. Epidemiology**

**2. Historical overview**

150 Skin Biopsy - Diagnosis and Treatment

case of OLP-related oral carcinoma. [8]

**Figure 1.** Foliose lichens growing on rock

Ferdinand Ritter von Hebra (1816-1880), famed dermatologist and co-founder of the renowned Vienna School of Dermatology, is credited with the first scientific description of the skin disease, he termed leichen ruber planus (in 1860). [4] But it was the famed British Dermatologist, Erasmus Wilson (1809-1884), who originally used the term lichen planus in his publication in 1869, noting the disorder in a group of 50 patients. [5] Lichen planus obtained its name because of the lacy white lines that bear a close resemblance to the symbiont, lichen, a composite organism consisting of a fungus (the mycobiont) and a photosynthetic partner (the photobiont or phycobiont, usually, a green algae) living together in a symbiotic relationship, seen growing on rocks (Figure 1). However, Ferdinand Ritter von Hebra used the term "lichen" to denote skin lesions which are exclusively nodular, that is characterised by a macular-papular skin eruption, hence, terms such as lichen pilaris (better known as Keratosis pilaris), and lichen nitidus are still used for other skin diseas‐ es, whose appearance differs markedly from that of lichen planus. [4] Heinrich Köbner (1838–1904) described the phenomenon that bears his name in 1872, at a meeting of the Silesian Society for National Culture. Four years later (1876) he published a paper describ‐ ing his original patient describing the development of isomorphic pathologic lesions in response to trauma in previously uninvolved sites of patients with skin diseases, most often seen in patients with psoriasis, but also in eczema and lichen planus. [6] These new lesions are clinically and histopathologically identical to those in the diseased skin and/or muco‐ sa. Louis Frédéric Wickham (1861-1913) is acknowledged as the first to describe the characteristic, fine, white or grey lines known as Wickham's striae (striae is derived from Latin for groove) or dots seen on the top of the pruritic papular rash of lichen planus of the skin, and also seen with OLP. [7] In 1910 François Henri Hallopeau reported the first OLP is a common condition, with a prevalence of between 0.5-2.2% of the population. [1, 9] However, a recent review of epidemiological studies specific to OLP, found only one study as being the most useful, being the most free of error and bias and so, is regarded as the most reliable estimation of population prevalence of OLP, at least in European populations with a reported prevalence of 1.27%. [10, 11] However, OLP most frequently presents in women, aged 40 years and above, by a ratio of approximately 3:1 to 3:2 compared with men, of the same age.

### **2.2. Pathogenesis**

The oral mucosa appears to have a limited immunological repertoire, predominantly a lichenoid-type reaction. This is characterised by delayed-type IV hypersensitivity reaction, dominated by cytotoxic CD8+ T-lymphocyte induced apoptosis of the basal keratinocytes, being the final common immunopathological pathway due to variety of insults, such as the development of autoantibodies against self-antigens, interaction with allergens, such as various drugs or dental materials, viruses, namely Hepatitis C (HCV), trauma (mechanical and chemical) and even stress. [12] However, the specifics, including the precise triggering factors, remain unknown and elusive.

The mechanisms involved in the aetio-pathogenesis of OLP are multifactorial and likely to be synergistic:

