Causes
Bladder
Infection
Detrusor sphincter dyssynergia
Neurogenic bladder (commonly spinal cord damage, pelvic splanchic nerve damage, cauda equina syndrome,  pontine micturition or storage center lesions, demyelinating diseases or Parkinsons disease)
Iatrogenic (caused by medical treatment/procedure) scarring of the bladder neck (commonly from removal of indwelling catheters or cystoscopy operations)
Damage to the bladder

Prostate
Benign prostatic hyperplasia (BPH)
Prostate cancer and other pelvic malignancies
Prostatitis

Penile urethra
Congenital urethral valves
Phimosis or pinhole meatus
Circumcision
Obstruction in the urethra, for example a stricture (usually caused either by injury or STD), a metastasis or a precipitated pseudogout crystal in the urine
Pseudodyssynergia
STD lesions (gonorrhoea causes numerous strictures, leading to a "rosary bead" appearance, whereas chlamydia usually causes a single stricture)
Emasculation

Postoperative
Risk factors include

Age: Older people may have degeneration of neural pathways involved with bladder function and it can lead to an increased risk of postoperative urinary retention. The risk of postoperative urinary retention increases up to 2.11 fold for people older than 60 years. Medications: Anticholinergics and medications with anticholinergic properties, alpha-adrenergic agonists, opiates, nonsteroidal anti-inflammatories (NSAIDs), calcium-channel blockers and beta-adrenergic agonists, may increase the risk. Anesthesia: General anesthetics during surgery may cause bladder atony by acting as a smooth muscle relaxant. General anesthetics can directly interfere with autonomic regulation of detrusor tone and predispose people to bladder overdistention and subsequent retention. Spinal anesthesia results in a blockade of the micturition reflex. Spinal anesthesia shows a higher risk of postoperative urinary retention compared to general anesthesia. Benign prostatic hyperplasia: Men with benign prostatic hyperplasia are at an increased risk of acute urinary retention.
Smokers melanosis is seen with the naked eye as a brown to black pigmentation of the oral tissue i.e. the gums, cheeks or palate  as well as in larynx. It is most often seen in the lower labial gingiva of tobacco users. Most easily it is found in Caucasians, due to their lack of a genetically caused melanin pigmentation.The brown to black colour is melanin. In skin, melanin prevents harmful UV-light from reaching deeper, sensible parts of the tissue. If UV-light penetrates deep, some of the toxic substances due to the UV-light damage to the cells, are bound to melanin in the epithelial cells and travel with the ageing cells to the skin surface, where they are expelled from the tissue surface. In this way the melanocytes and keratinocytes together protect the tissue, with melanin serving as a toxic defence and cleaning agent. In the oral mucosa, where the ageing epithelial cells move faster to the surface compared to skin, a similar defence-mechanism seems to be present, cleaning the mucosa from different toxic chemicals penetrating the epithelium. Besides chemicals in tobacco  also antimalaria-drugs cause an oral pigmentation. Smokers melanosis is like the genetic melanin pigmentations, a defence-system in action. The microscope shows smokers melanosis to be characterized by a melanin hyperpigmentation of the lower part of the oral epithelium, similar to sun-tanned skin. The hyperpigmentation consists of melanin granules which have the shape and colour of "coffea beans".