Joiner's cancer
Oral Pathology

Author: mario alovisi
Date: 26/05/2007


Cancer of paranasal sinus and nasal cavity is a disease in which cancer cells are found in the tissues of the paranasal sinuses or nasal cavity.

  • it's malignant
  • cancer of the paranasal sinus and nasal cavity commonly starts in the cells that line the oropharynx
  • much less often, cancer of paranasal sinus and nasal cavity starts in the color making cells called melanocyties and it's called "melanoma"
  • if cancer starts in the connecting tissue, it's called "sarcoma"


  • it can occur during all the ages
  • cancer of paranasal sinuses is relatively uncommon (the incidence in non exposed population is 1 case on 100000 subjects, in woodworkers is 5-9 on 10000)
  • decrescent order of incidence in different sinuses:
    (sinuses are air filled cavities in the skull)
  1. maxillary sinus
  2. ethmoidal sinus
  3. frontal sinus
  4. sphenoid sinus
  • more incidence in China and Japan (less in USA)


A doctor should be seen for these problems:

  • blocked sinus that do not clear
  • sinus infections
  • nosebleeds
  • a lump or sore that doesn't heal inside the nose
  • frequent headhaches or sinus pain
  • swelling or other troubles with the eyes
  • pain in the upper teeth
  • dentures that no longer fit well



wood dust exposure is strongly associated with the induction of several diseases of the higher airways mainly among furniture production workers

  • rhinitis
  • sinusitis
  • cancer of the nasal cavity and paranasal sinus( the cancer is a development of a patological condition that starts like rhinitis and sinusitis)

the risk of adenocarcinoma is elevated in joiners and woodworkers in general (OR=16.3) and however in association with high level wood-dust exposure (OR=26.3)


Mechanism of pathology

Usually cancer develops from sinusitis:it is defined as inflammation of the sinuses.
The inflammation can be caused by infectious or non infectious triggers.
The inflammation leads to blockade of sinus ostia (the normal sinus drenage pathways), which in turn leads to mucus ritention,decreased mucociliary clearance and predisposition to bacterial growth.

    • allergic rhinitis (started by wood antigens and repeated many times)
    • nasal polyposis (caused by focal protrusions of inflammatory mucose with white cells)
    • wood chemicals
    • Particles deposition:wood dust particles develop different effects:
      • decreased mucociliary clearance
      • enhanced inflammatory reaction the situation develops through displasy
      • supported infection of different microrganism after the formation of small lesions in the mucose

However increased risk is caused by wood-dust rather than by simultaneous exposure to other substances such as formaldheyde or wood preservaties

    • virus
      • Rhinovirus (picornaviridae)
      • Paramyxovirus (paramyxoviridae)
      • Orthomyxovirus
      • Adenovirus
      • EBV (HHV4)
    • bacteria
      • S.Pneumoniae
      • H.Influenzae
      • S.AUREUS
      • Moraxella Catharralis
      • GRAM- anaerobics (from the teeth)
      • P.Aeruginosa
      • Enterobacter
    • fungi
      • rhizopus is the causal agent of mucormycosis(it is a ficomices parasitic of the wood) photo
      • rhizomucor
      • aspergillus:it produces aflatoxin, mitogillin and restrictocin(against RNAm)

The combined mucormicosis and aspergillosis is the most frequent display of fungal infection.

Biochemical predisponent factors

the cellular H+ pomp is indispensable for the acidification of the lysosomes.Whithout them macrophages can't digest the pathogenous.
Every factor that influence this mechanism is a risk factor for the develoment of the disease

  • [Fe+2]
  • ipotiroidism
  • H+ pomp inhibitors (omeprazolo)

The expression of H+ pomp is regulated by the concentration of vit D
Less vit D=less acidification

  • polimorphism
  • epatic functionality (Cirrhosis)
  • diet
  • sun (UV)
  • IL6 (it can lessen the plasmatic concentration of DPB (vit.D binding protein)

cholesterol is important for the inflammatory response


aspergillosis: this fungus produces mitogillin that increases inflammation (ipersensibility) involving igE antibodies

Complication of sinusitis

  • adenocarcinome
  • Pott tumor
  • meningitis
  • trombosis of cavernous sinus


  • amoxicillin
  • cephalosporins (no penicillin because of inadequate antimicrobial coverage)
  • topic intranasa steroids (to address the strong inflammatory component of this disease)
  • mycolytic agents
  • surgery (to clair sinus of chronic infection, inflammation and polyps)


2007-06-01T18:28:25 - Gianpiero Pescarmona

Istituto Superiore per la Prevenzione e la Sicurezza del Lavoro
Neoplasie Naso-Sinusali
Il Tumore dei Seni Nasali e Paranasali (TuNS) e' una Patologia Rara che
Colpisce nel Nostro Paese con un'Incidenza Pari ad un Caso Ogni 100.000
Residenti. Il Rischio di Ammalarsi Aumenta in Maniera Rilevante negli
Esposti per Motivi Professionali alle Sostanze Chimiche e nei Settori
Lavorativi Coinvolti.
In Particolare e' Bene Accertata la Relazione Causale fra Esposizione a
Polveri di Legno Duro e di Cuoio ad Adenocarcinoma del Naso. Il Ruolo
Eziologico dei Composti di Nichel e Cromo e della Formaldeide e' Suggerito
da Numerosi Lavori ed Oggetto di un Ampio Dibattito Scientifico
- La Sorveglianza Epidemiologica dei Tumori Professionali
- Le Attivita' di Sorveglianza dei TuNS (Toscana)
- Le Attivita' di Sorveglianza dei TuNS (Lombardia)
- Ricerca Attiva dei TuNS in Fase Precoce nei Gruppi ad Alto Rischio (Marche)
- Fattori di Rischio Occupazionale per i TuNS
- La Diagnosi di TuNS
- Sorveglianza - Prevenzione e Indennizzo dei TuNS (Brescia)
Dimensione Del File PDF = 37 MB - Pagine = 249

2007-05-30T16:31:49 - mario alovisi

The want of Fe+2 has two mechanisms of damage:

  1. Hif >VEGF and it causes edema
  2. >receptor of transferrin (downregulation) and the consequence is that the cells grow quickly with Fe+2

the bacteric infections can be pathologically prominent also for that mechanism.( first of all the infection of EBV, CMV or HHV in general that lower greatly the plasmatic level of Fe+2)

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