Dermal reaction patterns end up causing the red non-scaly skin diseases.
The mnemonic for these is CUL DVA EVIE and the diseases are cellulitis, urticaria, L for lupus usually the subacute tumour type, possible light eruption and Lues or syphilis. The D is for drug reaction. The A is for annular erythema. V is viral or bacterial exanthem. EVIE is E for erythema multiforme, V for vasculitis, I for infiltrates and the other E is for erythema nodosum.
The thing about all these conditions is that the histological action takes place in the dermis and the epidermis isn't involved to any significant extent at all. This is true in most of these disorders. However an exception is where you have damage occurring at the interface of the dermal/epidermal junction. If enough damage occurs here then the epidermis itself can be damaged and epidermal changes can then occur, ranging from pseudo blister to actual scale.The classic condition that will do this is erythema multiforme. Other conditions with damage at the dermal/epidermal junction include graft versus-host disease and some of the autoimmune disorders such as dermatomyositis and acute lupus erythematosus. Lichen planus will also give basal layer damage but there is usually a very marked and significant lichenoid infiltrate of lymphocytes. This may not be the case in erythema multiforme or lupus.
However at this stage let's get back to the histopathology of the other red non-scaly disorders and we will slowly work our way through these before looking at the specific histological reaction patterns that we see in the dermis.
First of all you have your interface reaction pattern with damage at the dermal/epidermal junction and vacuolar degeneration of the basal keratinocytes.
Then you have the lichenoid pattern with a thick infiltrate of lymphocytes strongly apposed to the basement membrane.
Next you have the superficial and deep perivascular reaction pattern as the name implies involving the vessels of the superficial and deep perivascular plexus
The vasculitic reaction pattern is more than just the superficial and deep perivascular changes but involves inflammation and damage in and around major vessels and includes conditions such as leukocytoclastic vasculitis and polyarteritis nodosa..
Lastly there is a granulomatous reaction pattern in the dermis. This is deep and can be infective or non-infective.
Before we start that, the other thing that can obviously happen in the dermis is that you can have hyperproliferation of cells that are normally found there such as fibroblasts or adnexal structures such as hair follicles or sweat glands and this can give rise to a multitude of tumours that can arise in the dermis. Tumours can also arise from the nerves, both the nerve sheaths and the nerve axonal structure itself. Also from muscle, both the smooth muscle of the erector pili muscles and the deeper striated muscle, and also from the blood vessels.
There are a wide variety of tumours that can occur from each of these structures both benign and malignant and we will look at those in some detail later on. It will be obvious when you look under a microscope which of these structures you are dealing with, except if you have a lot of spindle cells which can be derived from melanocytes, keratinocytes, nerve cells and muscle cells. Special immunoperoxidase stains are required to determine the cell of origin.
When we look at dermal diseases we are looking at anything that is involving the dermal epidermal junction and below as far as the fat layer. Classically the reaction patterns have then be divided into those that involve a band like infiltrate at the dermal epidermal junction, which is known as a lichenoid infiltrate, those that have more sparse infiltrate but primarily damage to the cells of the dermal epidermal junction, which is then called interface damage and those that have collections of cells in the actual dermis itself. These cells can be eosinophils, neutrophils, lymphocytes, melanocytes or nevus cells and rarely cells from metastatic disease.
You can get granulomas occurring and you can obviously get tumours in the dermis where you get hyperproliferation of other tissue cells that are there. These can be tumours of fibroblasts, nerve or muscle cells and also those derived from hair follicles or eccrine and apocrine glands.
Most of the pathologies that involve the dermis will give red, non-scaly lesions or skin coloured non-scaly lesions and the fact that tyey are non-scaly indicates that the epidermis isn't going to be involved. So, if you see that most of the pathology is in the dermis then consider that the clinical morphology is going to be a non-scaly either red or skin coloured lesion. We will show you examples of that when we look at conditions such as granuloma annulare or even some of the atypical mycobacteria or deep fungal infections. Remember though that sometimes dermal processes can perforate the epidermis. They can go up through the epidermis as the body tries to get rid of the abnormal tissue. In those circumstances there will be epidermal involvement and this certainly has to be considered when a dermal process has an epidermal component as well.
Most of the pathologies that involve the dermis will give red, non-scaly lesions or skin coloured non-scaly lesions and the fact that tyey are non-scaly indicates that the epidermis isn't going to be involved. So, if you see that most of the pathology is in the dermis then consider that the clinical morphology is going to be a non-scaly either red or skin coloured lesion. We will show you examples of that when we look at conditions such as granuloma annulare or even some of the atypical mycobacteria or deep fungal infections. Remember though that sometimes dermal processes can perforate the epidermis. They can go up through the epidermis as the body tries to get rid of the abnormal tissue. In those circumstances there will be epidermal involvement and this certainly has to be considered when a dermal process has an epidermal component as well.
